灵龟八法治疗冠心病心绞痛的临床研究
|
摘要
目的
冠心病是冠状动脉粥样硬化性心脏病的简称,是粥样硬化斑块形成于冠状动脉内壁,导致血管腔的狭窄或梗阻,使血流受阻,心肌缺血、缺氧,甚至坏死,故又称缺血性心脏病。
冠心病属中医“胸痹”、“心痛”、“真心痛”等范畴,针刺治疗冠心病心绞痛操作简易与西药相比具有无毒性、无副作用、疗效高等特点,有广阔发展前景和意义。但对于采用灵龟八法治疗冠心病却鲜有报导。本文采用随机对照临床研究,观察通过灵龟八法按时开穴+辨证取穴组在改善冠心病患者临床症状,减轻心绞痛程度及发作频率,改善心电图缺血状态,抑制冠状动脉炎症反应,降低HCY水平方面的作用。
数据与方法
根据纳入标准及排除标准选取2012年3月1至2012年12月31日在深圳市中医院心血管内科住院诊断为冠心病心绞痛患者共160例。
(一)纳入标准：(1)有典型心绞痛发作症状。(2)心电图有明显的心肌缺血改变。(3)年龄40岁-80岁,心电图运动试验阳性或已确认为冠心病的患者。(4)符合冠心病诊断标准(参照国际心脏病学会和协会及世界卫生组织临床命名标准化联合专题组报告《缺血性心脏病的命名和诊断标准》拟定)；(5)自愿参加并已经签署知情同意书者。
(二)排除标准：(1)不符合诊断标准或不符合中医辨证属肾虚痰瘀互结之胸痹者；(2)重度心脑血管疾病患者：如心衰(心功能Ⅲ级以上)、急性心梗合并休克或心机功能Ⅲ级以上、急性脑梗塞合并昏迷或休克、急性脑出血等情况；(3)合并感染者：(4)严重肝肾功能不全者；(5)合并其它严重疾病者,如恶性肿瘤、重度营养不良、精神障碍；(6)妊振妇女；(7)不能配合试验擅自加减药物或中途退出者。
实验方法及步骤
将160例确诊为冠心病心绞痛标准的患者按照随机数字表随机分为4组：(1)治疗组：灵龟八法按时开穴+辨证取穴针刺治疗,每日1次,每次30分钟,七日为一疗程,共二疗程14次。(2)对照组A(灵龟八法开穴对照组)：灵龟八法按时开穴针刺治疗,每1次,每次30分钟,七日为一疗程。共二疗程14次。(3)对照组B(辨证取穴对照组)：辨证取穴针刺治疗,每1次,每次30分钟,七日为一疗程。共二疗程14次。(4)对照组C(空白对照组)：无需针刺治疗。全部病例疗程2周,均由医院营养食堂提供相同配餐。
观察治疗前,治疗2周后相关症状和体征,不良反应及高敏C反应蛋白(hs-CRP)(?)(?)同型半胱氨酸(HCY)的变化。HCY的检测：采用双抗体夹心酶联免疫吸附(ELISA)法检测；hs-CRP采用固相、化学发光免疫量度检测。数据用均数±标准差表示,以统计软件进行统计分析。计数资料采用X2检验,计量资料采用方差分析。
结果：
(一)疾病临床疗效比较
观察治疗前和治疗二周后患者临床症状、体征、心电图及血脂等检查结果,治疗二周后总有效例数经卡方检验：治疗组T与对照组C比较P<0.001,有非常显著性差异：治疗组T与对照组A、对照组B比较P<0.05,有显著性差异；对照组A、对照组B与对照组C比较P<0.05,有显著性差异；对照组A与对照组B比较P>0.05,无显著性差异。
(二)中医临床症状疗效比较
各组治疗后比较：治疗组T与对照组C比较P<0.001,有非常显著性差异；治疗组T与对照组A、对照组B比较P<0.05,有显著性差异；对照组A、对照组B与对照组C比较P<0.05,有显著性差异；对照组A与对照组B比较P>0.05,无显著性差异。
(三)心绞痛发作情况比较
1.心绞痛发作次数比较
各组治疗后比较：治疗组与对照组A、对照组B、对照组C比较P<0.05,有显著性差异；对照组A与对照组B比较P>0.05,无显著性差异；对照组A与对照组C比较P<0.05,有显著性差异；对照组B与对照组C比较P>0.05,无显著性差异。
2.心绞痛持续时间比较
各组治疗后比较：治疗组与对照组A、对照组B、对照组C比较P<0.05,有显著性差异；对照组A与对照组B比较P>0.05,无显著性差异；对照组A、对照组B与对照组C比较P<0.05,有显著性差异。
(四)治疗前后心功能比较
治疗组与对照组A、对照组B、对照组C比较P<0.05,有显着性差异；对照组A、对照组B与对照组C比较P<0.05,有显着性差异；对照组A与对照组B比较P>0.05,无显着性差异。
(五)高敏性C反应蛋白变化比较
治疗组与对照组A、对照组B、对照组C比较P<0.05,有显着性差异；对照组A、对照组B与对照组C比较P>0.05,无显着性差异；对照组A与对照组B比较P>0.05,无显着性差异。
(六)同型半胱氨酸变化比较
治疗组与对照组A、对照组B、对照组C比较P<0.05,有显着性差异；对照组A、对照组B与对照组C比较<0.05,有显着性差异；对照组A与对照组B比较P>0.05,无显着性差异。
结论
通过对160例冠心病患者随机对照临床研究,观察和分析,可初步得出以下结论：从总体疗效方面看来,灵龟八法+辨症取穴(T)具有显着性疗效,它优于对照组A及对照组B,可以明显改善冠心病之症状。本研究结果显示：灵龟八法+辨证取穴组具有良好的改善冠心病患者临床症状,减轻心绞痛程度及发作频率改善心电图缺血状态,抑制冠状动脉炎症反应,降低HCY水平的作用。这可能是灵龟八法+辨证取穴组治疗冠心病的现代医学机理之一。
讨论
灵龟八法治疗冠心病作用机理分析
冠心病(CHD)是冠状动脉粥样硬化性心脏病的简称,是粥样硬化块形成于冠状动脉内壁,导致血管的狭窄或梗阻,使血流受阻,心肌缺血、缺氧,甚至杯死,故又称缺血性心脏病。CHD是冠状动脉供血不足,心肌急剧的暂时的缺血与缺氧所引起的临床综合征。冠心病心绞痛属祖国中医学“胸痹”范畴。胸痹之病机为正气亏虚,痰浊、瘀血、气滞、寒凝,热郁等痹阻心脉,心失所养。胸痹心痛虽为本虚标实,虚实夹杂之病,然本虚为其根本。胸痹是指胸闷痛,甚则胸痛彻背,气短、喘息不得卧为主症的一种疾病。胸痹心痛发病多见于中老年人及绝经期以后的妇女,且多数胸痹心痛患者都兼有肾虚的临床表现。多因肾气亏虚日久导致肾阳亏虚,肾阳虚不能温煦心脾,致心阳,脾阳虚损,气化及温煦功能失司,使痰瘀内生,阻滞心脉而发病。肾阳亏虚和心脉瘀阻是胸痹心痛发病的主要因素。灵龟八法+辨证取穴治疗冠心病就是以这一基本病理特点为基础去治疗冠心病心绞痛及伴随症状。
灵龟八法理论基础
灵龟八法是时间针灸学的重要组成部分,其运用古代的九宫八卦学说,结合人体奇经八脉气血的会合,取十二经脉与奇经八脉相通的八脉会穴(公孙、内关、足临泣、外关、列缺、照海、后溪、申脉八穴)。八脉交会之所以能治疗多种疾病,主要机理在于八穴与奇经八脉存在着特殊的交会关系。奇经八脉在脏腑经络系统中占有重要的地位,《难经》曰：[脉有奇经八脉者,不拘于十二经],[比于从人图设沟渠,沟渠满溢,流于深湖]。把十二经脉比作江河沟渠,把奇经八脉比作湖泊。奇经八脉与十二正经通过穴位而相交。灵龟八法所用的穴位正是十经脉与奇经八脉相通的8个穴位,按时辰开穴针刺这些穴位既可以调节人体生物钟的节律,又调节经脉气血的流注,有效地达到治病的目的,故运用灵龟八法按时开穴治疗冠心病可以获得更好的疗效。谢感共教授以穴位导电量为指标,分别在不同季节系统测量灵龟八法穴位在“开”“闭”状态的导电量。结果开穴时穴位导电明显大于闭穴时导电量,认为灵龟八法穴位的“开”“闭”确实有其内在基础,其导电量的变化反映了开穴时的“气血旺盛”,闭穴时的“气血衰减”。多项临床和实验研究结果证实。本研究结果表明,灵龟八法治疗组疗效明显优于对照组(A,B,C)。尤其在临床诊效具有更大的优势。本研究结果再一次证明了穴位的开阖及八脉交会穴在针刺治疗中的重要作用。
配穴特点
窦汉卿《针经指南》记载：[公孙二穴……合内关穴。」、[临泣二穴……亦合于外关。」、[后溪二穴……合申脉。」、[照海二穴……合列缺]。这说明八穴之中存在着两两相合的关系。因此灵龟八法在临床上能够有效地治疗冠心病及伴随症状。且体现了中医学的“天人合一”的观点。
Objective
Coronary Heart Disease (CHD) is the narrowing or blockage of the coronary arteries, usually caused by atherosclerosis. Atherosclerosis is the buildup of cholesterol and fatty deposits on the inner walls of the arteries. These plaques can restrict blood flow to the heart muscle, leading to lack of oxygen supply even death of tissue. It is also called Ischemic Heart Disease.
CHD in Traditional Chinese Medicine (TCM) terms are "chest paralysis","heart pain","heart pumping","real heart pain". The acupuncture method is easy to use and it is better than western medicine because it contains no drugs and no side effect in treating CHD. The effectiveness of acupuncture has a greater prospect but in combination of Ling Gui Ba Fa to treat CHD is seldom mentioned.
This thesis is a RCT clinical study. Through Ling Gui Ba Fa to chose the standard acupoints and symptom related Chinese medicine, compare the blood flow in coronary artery, release CHD chest pain and frequency, improve ECG output, reduce coronary artery inflammation, reduce thrombocytes activation, lower HCY level.
Data and Method
According to the standard selection,160CHD confirmed patients in Shenzhen TCM Hospital are chosen during1/3/2012to31/12/2012.
1. Standard of acceptance:
a. Have typical CHD or myocardial infarction symptoms.
b. ECG confirmed lack of heart blood flow.
c. Age between40to80, ECG confirmed CHD.
d. Meet the CHD diagnosis standard according to International Cardiology Congress and WHO.
e. Voluntary and signed the agreement of consent.
2. Standard of rejection:
a. Not meet the diagnosis symptom or in the field of TCM "chest paralysis"
b. Severe heart brain vessel patient such as heart failure, heart attack with shock or coma, brain bleeding.
c. Combined infection.
d. Severe liver and kidney function failure.
e. Other severe illness such as tumor, lack of nutrition, mental disorder.
f. In pregnancy.
g. Not follow the clinical trail or those quitted.
Trail Method and Procedure
Randomly divide the160patients into4groups:
1. Therapy group
Acupuncture according to Ling Gui Ba Fa to chose the acupoints, plus symptom related acupoints. Once daily,30minutes each time,7days as1cycle. Apply2cycles for a total of14days.
2. Control group A
Acupuncture according to Ling Gui Ba Fa to chose the acupoints only. Once daily,30minutes each time,7days as1cycle. Apply2cycles for a total of14days.
3. Control group B
Acupuncture according to symptom related acupoints. Once daily,30minutes each time,7days as1cycle. Apply2cycles for a total of14days.
4. Control Group C
Blank control, no acupuncture applied.
All patients were given the same food and drink from the hospital for the2weeks of trial.
Record the result before and after the trial, including the adverse effect and the serum level of hs-CRP and HCY. HCY use enzyme linked immunosorbent assay (ELISA), hs-CRP use solid phase chemiluminescence immunization, statistical use SPSS15.0for windows and X2test.
Result
1. Clinical Result Comparison
Before and after treatment, the clinical symptoms, body conditions, ECG and blood fats are compared. X2test showed that therapy group T has very significant difference with control group C (P<0.001).
Therapy group T has significant difference with control group A and control group B (P<0.05).
Control group A and control group B have significant difference with control group C (P<0.05).
Control group A has no significant difference with control group B (P>0.05).
2. TCM Clinical Result Comparison
After the treatment, results showed that therapy group T has very significant difference with control group C (P<0.001).
Therapy group T has significant difference with control group A and control group B (P<0.05).
Control group A and control group B have significant difference with control group C (P<0.05).
Control group A has no significant difference with control group B (P>0.05).
3. Angina Pectoris Condition Comparison
a. Frequency of angina pectoris
After the treatment, results showed that therapy group T has significant difference with control group A, control group B and control group C (P<0.05).
Control group A has significant difference with control group C (P<0.05).
Control group B has no significant difference with control group C (P>0.05).
Control group A has no significant difference with control group B (P>0.05).
b. Duration of angina pectoris
After the treatment, results showed that therapy group T has significant difference with control group A, control group B and control group C (P<0.05).
Control group A has no significant difference with control group B (P>0.05).
Control group A and control group B have significant difference with control group C (P<0.05).
4. Heart Function Comparison
After the treatment, results showed that therapy group T has significant difference with control group A, control group B and control group C (P<0.05).
Control group A and control group B have significant difference with control group C (P<0.05).
Control group A has no significant difference with control group B (P>0.05).
5. hs-CRP Comparison
After the treatment, results showed that therapy group T has significant difference with control group A, control group B and control group C (P<0.05).
Control group A and control group B have no significant difference with control group C (P>0.05).
Control group A has no significant difference with control group B (P>0.05).
6. HCY Comparison
After the treatment, results showed that therapy group T has significant difference with control group A, control group B and control group C (P<0.05).
Control group A and control group B have significant difference with control group C (P<0.05).
Control group A has no significant difference with control group B (P>0.05).
Conclusion
Through the160cases clinical study of coronary heart disease with angina cordis, acupuncture according to Ling Gui Ba Fa to chose the acupoints plus symptom related acupoints has better result than the others.
The results are reflected by:lessen the angina degree and frequency, improve blood flow as shown in ECG, inhibit inflammation in coronary artery, inhibit platelet activation, lower HCY level. Acupuncture according to Ling Gui Ba Fa plus symptom related acupoints is better than only using Ling Gui Ba Fa because more acupoints can be used. The typical examples are Tan Zhong Xue and Xin Shu Xue. This maybe the good result in lessen the angina degree and frequency, improve blood flow as shown in ECG, inhibit inflammation in coronary artery, inhibit platelet activation, lower HCY level symptom.
Discussion
The mechanism of Ling Gui Ba Fa on coronary heart disease (CHD). CHD is the narrowing or blockage of the coronary arteries, usually caused by atherosclerosis. Atherosclerosis is the buildup of cholesterol and fatty deposits on the inner walls of the arteries. These plaques can restrict blood flow to the heart muscle, leading to lack of oxygen supply even death of tissue. It is also called Ischemic Heart Disease. CHD reflects lack of blood flow in coronary artery. This lack of blood or oxygen leads to a series of clinical symptoms.
CHD in Traditional Chinese Medicine (TCM) terms are "chest paralysis" The cause of this is the body weakness, lack of energy inside the body, low circulation, poor temperature regulation, accumulation of body waste. The symptom can be severe but the root cause is body weakness. This is why CHD is more on the elderly or women after menopause. At that age, the kidney function lowered. The power from kidney to heart becomes less. This leads to a series of heart problem. So the main factor of CHD is the kidney and heart.
Acupuncture according to Ling Gui Ba Fa plus symptom related acupoints can deal with this main factor. Improving kidney and heart can cure the coronary heart disease with angina cordis and the accompanying symptoms.
A. Basic theory
Ling Gui Ba Fa is a timing method to choose acupuncture point in the human body to cure a definite diseases or symptoms. It fits with the meridians system and the function between them. The8acupoints that come across the meridian with main function are Gong Sun, Nei Guan, Zu Lin Qi, Wai Guan, Lie Que, Zhao Hai, Hou Xi, Shen Mai. The origin of this system is very ancient.
"Nan Jing" mentioned:meridian is a channel or river, the acupoint is like a lake. So the come across function of the8acupoints can regulate the circulation within the body, like a lake regulates the flow in the river. But the flow is time depended. This is just fit to the timing method of Ling Gui Ba Fa. The timing is similar to the human biological clock. The "close" or "open" of the acupoint reflects the flow volume and can be detected by conduct ivy meter. In the stage of "open", blood flow increase. In the stage of "close", blood flow decrease. By method of benefiting in suitable acupoint in "open" stage, the weakness can be lessened.
In this clinical trial, the result of the therapy group is significantly better the control group A, B, and C. This reflects the characteristic of the8acupoint and the Ling Gui Ba Fa has a very important function in the acupuncture treatment.
B. Characteristics of acupoint combination
Dou Han Qing "Zhen Jing Zhi Nan" said:Gong Sun…can use with Nei Guan; Zu Lin Qi…with Wai Guan; Hou Xi…with Shen Mai; Zhao Hai…with Lie Que. This explains the combination and function between the pairing acupoints. The timing is the human to communicate with the nature. Ling Gui Ba Fa fits this point of view and can effectively treat the CHD and the accompanying symptoms.
冠心病是冠状动脉粥样硬化性心脏病的简称,是粥样硬化斑块形成于冠状动脉内壁,导致血管腔的狭窄或梗阻,使血流受阻,心肌缺血、缺氧,甚至坏死,故又称缺血性心脏病。
冠心病属中医“胸痹”、“心痛”、“真心痛”等范畴,针刺治疗冠心病心绞痛操作简易与西药相比具有无毒性、无副作用、疗效高等特点,有广阔发展前景和意义。但对于采用灵龟八法治疗冠心病却鲜有报导。本文采用随机对照临床研究,观察通过灵龟八法按时开穴+辨证取穴组在改善冠心病患者临床症状,减轻心绞痛程度及发作频率,改善心电图缺血状态,抑制冠状动脉炎症反应,降低HCY水平方面的作用。
数据与方法
根据纳入标准及排除标准选取2012年3月1至2012年12月31日在深圳市中医院心血管内科住院诊断为冠心病心绞痛患者共160例。
(一)纳入标准：(1)有典型心绞痛发作症状。(2)心电图有明显的心肌缺血改变。(3)年龄40岁-80岁,心电图运动试验阳性或已确认为冠心病的患者。(4)符合冠心病诊断标准(参照国际心脏病学会和协会及世界卫生组织临床命名标准化联合专题组报告《缺血性心脏病的命名和诊断标准》拟定)；(5)自愿参加并已经签署知情同意书者。
(二)排除标准：(1)不符合诊断标准或不符合中医辨证属肾虚痰瘀互结之胸痹者；(2)重度心脑血管疾病患者：如心衰(心功能Ⅲ级以上)、急性心梗合并休克或心机功能Ⅲ级以上、急性脑梗塞合并昏迷或休克、急性脑出血等情况；(3)合并感染者：(4)严重肝肾功能不全者；(5)合并其它严重疾病者,如恶性肿瘤、重度营养不良、精神障碍；(6)妊振妇女；(7)不能配合试验擅自加减药物或中途退出者。
实验方法及步骤
将160例确诊为冠心病心绞痛标准的患者按照随机数字表随机分为4组：(1)治疗组：灵龟八法按时开穴+辨证取穴针刺治疗,每日1次,每次30分钟,七日为一疗程,共二疗程14次。(2)对照组A(灵龟八法开穴对照组)：灵龟八法按时开穴针刺治疗,每1次,每次30分钟,七日为一疗程。共二疗程14次。(3)对照组B(辨证取穴对照组)：辨证取穴针刺治疗,每1次,每次30分钟,七日为一疗程。共二疗程14次。(4)对照组C(空白对照组)：无需针刺治疗。全部病例疗程2周,均由医院营养食堂提供相同配餐。
观察治疗前,治疗2周后相关症状和体征,不良反应及高敏C反应蛋白(hs-CRP)(?)(?)同型半胱氨酸(HCY)的变化。HCY的检测：采用双抗体夹心酶联免疫吸附(ELISA)法检测；hs-CRP采用固相、化学发光免疫量度检测。数据用均数±标准差表示,以统计软件进行统计分析。计数资料采用X2检验,计量资料采用方差分析。
结果：
(一)疾病临床疗效比较
观察治疗前和治疗二周后患者临床症状、体征、心电图及血脂等检查结果,治疗二周后总有效例数经卡方检验：治疗组T与对照组C比较P<0.001,有非常显著性差异：治疗组T与对照组A、对照组B比较P<0.05,有显著性差异；对照组A、对照组B与对照组C比较P<0.05,有显著性差异；对照组A与对照组B比较P>0.05,无显著性差异。
(二)中医临床症状疗效比较
各组治疗后比较：治疗组T与对照组C比较P<0.001,有非常显著性差异；治疗组T与对照组A、对照组B比较P<0.05,有显著性差异；对照组A、对照组B与对照组C比较P<0.05,有显著性差异；对照组A与对照组B比较P>0.05,无显著性差异。
(三)心绞痛发作情况比较
1.心绞痛发作次数比较
各组治疗后比较：治疗组与对照组A、对照组B、对照组C比较P<0.05,有显著性差异；对照组A与对照组B比较P>0.05,无显著性差异；对照组A与对照组C比较P<0.05,有显著性差异；对照组B与对照组C比较P>0.05,无显著性差异。
2.心绞痛持续时间比较
各组治疗后比较：治疗组与对照组A、对照组B、对照组C比较P<0.05,有显著性差异；对照组A与对照组B比较P>0.05,无显著性差异；对照组A、对照组B与对照组C比较P<0.05,有显著性差异。
(四)治疗前后心功能比较
治疗组与对照组A、对照组B、对照组C比较P<0.05,有显着性差异；对照组A、对照组B与对照组C比较P<0.05,有显着性差异；对照组A与对照组B比较P>0.05,无显着性差异。
(五)高敏性C反应蛋白变化比较
治疗组与对照组A、对照组B、对照组C比较P<0.05,有显着性差异；对照组A、对照组B与对照组C比较P>0.05,无显着性差异；对照组A与对照组B比较P>0.05,无显着性差异。
(六)同型半胱氨酸变化比较
治疗组与对照组A、对照组B、对照组C比较P<0.05,有显着性差异；对照组A、对照组B与对照组C比较<0.05,有显着性差异；对照组A与对照组B比较P>0.05,无显着性差异。
结论
通过对160例冠心病患者随机对照临床研究,观察和分析,可初步得出以下结论：从总体疗效方面看来,灵龟八法+辨症取穴(T)具有显着性疗效,它优于对照组A及对照组B,可以明显改善冠心病之症状。本研究结果显示：灵龟八法+辨证取穴组具有良好的改善冠心病患者临床症状,减轻心绞痛程度及发作频率改善心电图缺血状态,抑制冠状动脉炎症反应,降低HCY水平的作用。这可能是灵龟八法+辨证取穴组治疗冠心病的现代医学机理之一。
讨论
灵龟八法治疗冠心病作用机理分析
冠心病(CHD)是冠状动脉粥样硬化性心脏病的简称,是粥样硬化块形成于冠状动脉内壁,导致血管的狭窄或梗阻,使血流受阻,心肌缺血、缺氧,甚至杯死,故又称缺血性心脏病。CHD是冠状动脉供血不足,心肌急剧的暂时的缺血与缺氧所引起的临床综合征。冠心病心绞痛属祖国中医学“胸痹”范畴。胸痹之病机为正气亏虚,痰浊、瘀血、气滞、寒凝,热郁等痹阻心脉,心失所养。胸痹心痛虽为本虚标实,虚实夹杂之病,然本虚为其根本。胸痹是指胸闷痛,甚则胸痛彻背,气短、喘息不得卧为主症的一种疾病。胸痹心痛发病多见于中老年人及绝经期以后的妇女,且多数胸痹心痛患者都兼有肾虚的临床表现。多因肾气亏虚日久导致肾阳亏虚,肾阳虚不能温煦心脾,致心阳,脾阳虚损,气化及温煦功能失司,使痰瘀内生,阻滞心脉而发病。肾阳亏虚和心脉瘀阻是胸痹心痛发病的主要因素。灵龟八法+辨证取穴治疗冠心病就是以这一基本病理特点为基础去治疗冠心病心绞痛及伴随症状。
灵龟八法理论基础
灵龟八法是时间针灸学的重要组成部分,其运用古代的九宫八卦学说,结合人体奇经八脉气血的会合,取十二经脉与奇经八脉相通的八脉会穴(公孙、内关、足临泣、外关、列缺、照海、后溪、申脉八穴)。八脉交会之所以能治疗多种疾病,主要机理在于八穴与奇经八脉存在着特殊的交会关系。奇经八脉在脏腑经络系统中占有重要的地位,《难经》曰：[脉有奇经八脉者,不拘于十二经],[比于从人图设沟渠,沟渠满溢,流于深湖]。把十二经脉比作江河沟渠,把奇经八脉比作湖泊。奇经八脉与十二正经通过穴位而相交。灵龟八法所用的穴位正是十经脉与奇经八脉相通的8个穴位,按时辰开穴针刺这些穴位既可以调节人体生物钟的节律,又调节经脉气血的流注,有效地达到治病的目的,故运用灵龟八法按时开穴治疗冠心病可以获得更好的疗效。谢感共教授以穴位导电量为指标,分别在不同季节系统测量灵龟八法穴位在“开”“闭”状态的导电量。结果开穴时穴位导电明显大于闭穴时导电量,认为灵龟八法穴位的“开”“闭”确实有其内在基础,其导电量的变化反映了开穴时的“气血旺盛”,闭穴时的“气血衰减”。多项临床和实验研究结果证实。本研究结果表明,灵龟八法治疗组疗效明显优于对照组(A,B,C)。尤其在临床诊效具有更大的优势。本研究结果再一次证明了穴位的开阖及八脉交会穴在针刺治疗中的重要作用。
配穴特点
窦汉卿《针经指南》记载：[公孙二穴……合内关穴。」、[临泣二穴……亦合于外关。」、[后溪二穴……合申脉。」、[照海二穴……合列缺]。这说明八穴之中存在着两两相合的关系。因此灵龟八法在临床上能够有效地治疗冠心病及伴随症状。且体现了中医学的“天人合一”的观点。
Objective
Coronary Heart Disease (CHD) is the narrowing or blockage of the coronary arteries, usually caused by atherosclerosis. Atherosclerosis is the buildup of cholesterol and fatty deposits on the inner walls of the arteries. These plaques can restrict blood flow to the heart muscle, leading to lack of oxygen supply even death of tissue. It is also called Ischemic Heart Disease.
CHD in Traditional Chinese Medicine (TCM) terms are "chest paralysis","heart pain","heart pumping","real heart pain". The acupuncture method is easy to use and it is better than western medicine because it contains no drugs and no side effect in treating CHD. The effectiveness of acupuncture has a greater prospect but in combination of Ling Gui Ba Fa to treat CHD is seldom mentioned.
This thesis is a RCT clinical study. Through Ling Gui Ba Fa to chose the standard acupoints and symptom related Chinese medicine, compare the blood flow in coronary artery, release CHD chest pain and frequency, improve ECG output, reduce coronary artery inflammation, reduce thrombocytes activation, lower HCY level.
Data and Method
According to the standard selection,160CHD confirmed patients in Shenzhen TCM Hospital are chosen during1/3/2012to31/12/2012.
1. Standard of acceptance:
a. Have typical CHD or myocardial infarction symptoms.
b. ECG confirmed lack of heart blood flow.
c. Age between40to80, ECG confirmed CHD.
d. Meet the CHD diagnosis standard according to International Cardiology Congress and WHO.
e. Voluntary and signed the agreement of consent.
2. Standard of rejection:
a. Not meet the diagnosis symptom or in the field of TCM "chest paralysis"
b. Severe heart brain vessel patient such as heart failure, heart attack with shock or coma, brain bleeding.
c. Combined infection.
d. Severe liver and kidney function failure.
e. Other severe illness such as tumor, lack of nutrition, mental disorder.
f. In pregnancy.
g. Not follow the clinical trail or those quitted.
Trail Method and Procedure
Randomly divide the160patients into4groups:
1. Therapy group
Acupuncture according to Ling Gui Ba Fa to chose the acupoints, plus symptom related acupoints. Once daily,30minutes each time,7days as1cycle. Apply2cycles for a total of14days.
2. Control group A
Acupuncture according to Ling Gui Ba Fa to chose the acupoints only. Once daily,30minutes each time,7days as1cycle. Apply2cycles for a total of14days.
3. Control group B
Acupuncture according to symptom related acupoints. Once daily,30minutes each time,7days as1cycle. Apply2cycles for a total of14days.
4. Control Group C
Blank control, no acupuncture applied.
All patients were given the same food and drink from the hospital for the2weeks of trial.
Record the result before and after the trial, including the adverse effect and the serum level of hs-CRP and HCY. HCY use enzyme linked immunosorbent assay (ELISA), hs-CRP use solid phase chemiluminescence immunization, statistical use SPSS15.0for windows and X2test.
Result
1. Clinical Result Comparison
Before and after treatment, the clinical symptoms, body conditions, ECG and blood fats are compared. X2test showed that therapy group T has very significant difference with control group C (P<0.001).
Therapy group T has significant difference with control group A and control group B (P<0.05).
Control group A and control group B have significant difference with control group C (P<0.05).
Control group A has no significant difference with control group B (P>0.05).
2. TCM Clinical Result Comparison
After the treatment, results showed that therapy group T has very significant difference with control group C (P<0.001).
Therapy group T has significant difference with control group A and control group B (P<0.05).
Control group A and control group B have significant difference with control group C (P<0.05).
Control group A has no significant difference with control group B (P>0.05).
3. Angina Pectoris Condition Comparison
a. Frequency of angina pectoris
After the treatment, results showed that therapy group T has significant difference with control group A, control group B and control group C (P<0.05).
Control group A has significant difference with control group C (P<0.05).
Control group B has no significant difference with control group C (P>0.05).
Control group A has no significant difference with control group B (P>0.05).
b. Duration of angina pectoris
After the treatment, results showed that therapy group T has significant difference with control group A, control group B and control group C (P<0.05).
Control group A has no significant difference with control group B (P>0.05).
Control group A and control group B have significant difference with control group C (P<0.05).
4. Heart Function Comparison
After the treatment, results showed that therapy group T has significant difference with control group A, control group B and control group C (P<0.05).
Control group A and control group B have significant difference with control group C (P<0.05).
Control group A has no significant difference with control group B (P>0.05).
5. hs-CRP Comparison
After the treatment, results showed that therapy group T has significant difference with control group A, control group B and control group C (P<0.05).
Control group A and control group B have no significant difference with control group C (P>0.05).
Control group A has no significant difference with control group B (P>0.05).
6. HCY Comparison
After the treatment, results showed that therapy group T has significant difference with control group A, control group B and control group C (P<0.05).
Control group A and control group B have significant difference with control group C (P<0.05).
Control group A has no significant difference with control group B (P>0.05).
Conclusion
Through the160cases clinical study of coronary heart disease with angina cordis, acupuncture according to Ling Gui Ba Fa to chose the acupoints plus symptom related acupoints has better result than the others.
The results are reflected by:lessen the angina degree and frequency, improve blood flow as shown in ECG, inhibit inflammation in coronary artery, inhibit platelet activation, lower HCY level. Acupuncture according to Ling Gui Ba Fa plus symptom related acupoints is better than only using Ling Gui Ba Fa because more acupoints can be used. The typical examples are Tan Zhong Xue and Xin Shu Xue. This maybe the good result in lessen the angina degree and frequency, improve blood flow as shown in ECG, inhibit inflammation in coronary artery, inhibit platelet activation, lower HCY level symptom.
Discussion
The mechanism of Ling Gui Ba Fa on coronary heart disease (CHD). CHD is the narrowing or blockage of the coronary arteries, usually caused by atherosclerosis. Atherosclerosis is the buildup of cholesterol and fatty deposits on the inner walls of the arteries. These plaques can restrict blood flow to the heart muscle, leading to lack of oxygen supply even death of tissue. It is also called Ischemic Heart Disease. CHD reflects lack of blood flow in coronary artery. This lack of blood or oxygen leads to a series of clinical symptoms.
CHD in Traditional Chinese Medicine (TCM) terms are "chest paralysis" The cause of this is the body weakness, lack of energy inside the body, low circulation, poor temperature regulation, accumulation of body waste. The symptom can be severe but the root cause is body weakness. This is why CHD is more on the elderly or women after menopause. At that age, the kidney function lowered. The power from kidney to heart becomes less. This leads to a series of heart problem. So the main factor of CHD is the kidney and heart.
Acupuncture according to Ling Gui Ba Fa plus symptom related acupoints can deal with this main factor. Improving kidney and heart can cure the coronary heart disease with angina cordis and the accompanying symptoms.
A. Basic theory
Ling Gui Ba Fa is a timing method to choose acupuncture point in the human body to cure a definite diseases or symptoms. It fits with the meridians system and the function between them. The8acupoints that come across the meridian with main function are Gong Sun, Nei Guan, Zu Lin Qi, Wai Guan, Lie Que, Zhao Hai, Hou Xi, Shen Mai. The origin of this system is very ancient.
"Nan Jing" mentioned:meridian is a channel or river, the acupoint is like a lake. So the come across function of the8acupoints can regulate the circulation within the body, like a lake regulates the flow in the river. But the flow is time depended. This is just fit to the timing method of Ling Gui Ba Fa. The timing is similar to the human biological clock. The "close" or "open" of the acupoint reflects the flow volume and can be detected by conduct ivy meter. In the stage of "open", blood flow increase. In the stage of "close", blood flow decrease. By method of benefiting in suitable acupoint in "open" stage, the weakness can be lessened.
In this clinical trial, the result of the therapy group is significantly better the control group A, B, and C. This reflects the characteristic of the8acupoint and the Ling Gui Ba Fa has a very important function in the acupuncture treatment.
B. Characteristics of acupoint combination
Dou Han Qing "Zhen Jing Zhi Nan" said:Gong Sun…can use with Nei Guan; Zu Lin Qi…with Wai Guan; Hou Xi…with Shen Mai; Zhao Hai…with Lie Que. This explains the combination and function between the pairing acupoints. The timing is the human to communicate with the nature. Ling Gui Ba Fa fits this point of view and can effectively treat the CHD and the accompanying symptoms.
引文
[1]黄仑,李忠汗,喻斌等.针药结合治疗冠心病研究进展.安徽医药杂志,2011；16(6)：664-665.
[2]罗陆一,冯润芬,吴泽民等.温肾化痰活血法心腧穴位外治治疗冠心病心绞痛观察.中医药学刊,2006；24(6)：984-985.
[3]黄梦雨,罗陆一.罗陆一教授治疗冠心病心绞痛经验介绍.新中医杂志,2009：41(11)：13-14.
[4]李磊针.炙时间治疗学.太原：山西科学技术出版社,1994；1.
[5]管遵惠.试论经气的运行.云南中医杂志,1985；3：18.
[6]史裕整理.灵枢经.沈阳：辽宁科学技术出版社,1997.
[7]王冰注.黄帝内经素问.北京：人民卫生出版社,1978.
[8]赵估.圣济总录.北京：人民卫生出版社,1998.
[9]林佩琴.类证治裁.北京：人民卫生出版社,1988.
[10]朱丹溪.丹溪心法.上海：上海科学出版社,1959.
[11]王肯堂.证治准绳.上海：上海科学技术出版社,1984.
[12]叶天士.临证指南医案.上海：上海科学技术出版社,1961.
[13]吴谦.医宗金鉴·订正金匮要略注[M].北京：人民卫生出版社,1982；2：523.
[14]李克光,杨百茀.金匮要略讲义[M].上海：上海科技出版社,1985；94.
[15]梅岩,张明雪.从“阳微阴弦”治冠心病[J].中医药学刊,2006；24(4)：683-684.
[16]张机.金匾要略方论.北京：人民卫生出版社,1978.
[17]赵估.圣济总录.北京：人民卫生出版社,1998.
[18]李十红,等.治疗冠状动脉痉挛心绞痛的经验.辽宁中医杂志,1997；(2)：5.
[19]罗粗文.胸痹心痛临床几个问题探讨.四川中医,1988；(2)：8.
[20]杨利.邓铁涛教授“冠心三论”[J].湖南中医药导报,2004,(6)：8-10.
[21]巢元方.诸病源候论.北京：人民卫生出版社,1984.
[22]林佩琴.类证治裁.北京：人民卫生出版社,1988.
[23]朱文锋.国家标准应用·中医内科疾病诊疗常规[M].长沙：湖南科技出版社,1998：247.
[24]焦树德,路志正.实用中医心病学[M].北京：人民卫生出版,1995；600-616.
[25]丁斗,董小君.气元论在胸痹心痛证治中的病因病机规律研究[J].长春中医药大学学报,2010；26(2)：160-170.
[26]徐健,敖杰男.浅谈痰瘀互结证与胸痹的关系[J].时珍国医国药,2008；18(5)：1229-1230.
[27]王伯东.张景凤自拟方治疗胸痹痰瘀互结证验案举隅[J].吉林中医药,2010； 30(1)：59.
[28]郑玲玲,王强.王强教授治疗痰瘀互结型胸痹临证经验[J].吉林中医药,2012；32(4)：333.
[29]林晓忠.邓铁涛老师调脾护心法治疗冠心病临床经验总结.中国医药学报,2002；17(1)：40.
[30]罗陆一.从肾论治冠心病机理例析.中医药学刊,2005；23(4)：58.
[31]罗粗文.胸痹心痛临床几个问题探讨.四川中医,1988；(2)：8.
[32]李淑贞,等.补肾活血化痰法治疗冠心病心绞痛浅议.实用中医药杂志,2004；20(9)：516.
[33]竺培华,秦志仁.补肾益气活血法治疗冠心病的临床观察.中成药,2004；26(5)：附11.
[34]张永健,俞荣青.对《冠心病(心绞痛、心肌梗塞)中医辨证试行标准》的几点意见[J].中西医结合杂志社,1985；(2)：128.
[35]中医研究院,广东中医学院.中医名词术语选择[M].北京：人民卫生出版社,1973；360.
[36]王永炎.中医内科学[M].上海：上海科技出版社,1997；108-109.
[37]岳美中.岳美中医案集[M].北京：人民卫生出版社,1978；68.
[38]冯润芬,罗陆一.通心贴心俞穴外敷治疗冠心病心绞痛60例临床观察.中国中医药科技,2005；12(1)：47-48.
[39]高彩霞,李冬玉,罗清菊,等.冠心贴膜对冠心病心绞痛患者部分凝血活酶时间和纤维蛋白原水平的影响.河南中医,2005；25(10)：31-32.
[40]龚信.古今医鉴[M].北京：中国中医药出版社,1997；294.
[41]陈寅生,李丽.心脉通贴剂中冰片的透皮吸收实验研究.河南大学学报(医学版),2006；25(1)：30-31.
[42]林晓忠,吴焕林,严夏.邓铁涛教授论治冠心病的规律探要[J].中医药学刊,2001：19(5)412-414.
[43]唐容川.中医内科名著集成[M].北京：华夏出版社,1998；887-888.
[44]黄绳武,宋宵宏.中药复方制剂心安康贴剂的透皮吸收促进剂选择研究.中国药师,2003；6(7)：391-393.
[45]沈建平,丁建花,张银娣,等.保心包贴膜对心肌缺血的影响.中国微循,2002：6(2)：87-91.
[46]张建文,汪大鹏,熊晓玲,等.复方丹参气雾剂治疗冠心病心绞痛的临床观察.湖北中医杂志,2005；27(1)：15-16.
[47]赵锡民.中医药防治肿瘤的研究[J].长春中医药大学学报,2012；28(1)：169-170.
[48]宋丽晶,刘建璇,毋英杰.速效活心气雾剂对麻醉犬心脏功能和血流动力学的影响.长春中医学院学报,2001；17(1)：36-37.
[49]杨发荣.心痛气雾剂治疗冠心病心绞痛100例.辽宁中医杂志,1997；24(8)：355.
[50]王安才,常宝华,杨尚印,等.保心包贴膜对稳定型心绞痛患者血浆内皮素和一氧化氮水平的影响.中国临床药理学与治疗学,2000；5(2)：145-146.
[51]黄伟,郑义通,胡世文.体外超声助溶治疗急性心肌梗死的效果观察.齐齐哈尔医学院学报,2002；23(10)：1108-1109.
[52]刘小斌.邓铁涛教授五脏相关学术源流探讨[J].广州中医药人学学报.2006；23(5)：424-425.
[53]林慧光主编。陈修｜元｜医学全書[M].北京：中国中医药出版社,2003；10：472-474.
[54]郝福庆.拿治疗冠心病70例.实用中医药杂志,2001；17(11)：29.
[55]程国彭.医学心悟[M].北京：人生出版社,2006；6：126.
[56]王兴,魏向春,姜波.血apoA-1,apoB水平与冠心病中医辨证关系的探讨.中医药学报,1991；(1)：46-48.
[57]程小曲.痰浊型冠心病与血脂、脂蛋白、载脂蛋白的关系及痰浊形成机理的探讨.新中医,1994；(3)：7-9.
[58]金志刚,周端,顾仁樾,等.冠心病血瘀证与血清脂蛋白(a)含量的临床观察.河南中医药学刊,1995；10(3)：28-29.
[59]朱晓岚,林院昌,崔志英,等.冠心病的中医辨证与甲皱微循环和血液流变学之间的相关性探讨.第一军医大学学报,1990；10(3)：225-227.
[60]赖真,郭恕,汪建红,等.冠心病心绞痛气虚血瘀和气滞血瘀的微循环变化.湖南中医学院学报,1994；14(3)：44-46.
[61]贾宝善,刘莉,马军,等.冠心病患者血小板膜糖蛋白及血小板功能与中医辨证分型关系的研究.中西医结合杂志,1989；9(12)：717-719.
[62]骆丽娟.冠心病证型与P—选择素、TXB 2及62—Keto—PGF1α含量变化关系的研究.上海中医药杂志,2002；(7)：13-14.
[63]黄文权,罗致强.冠心病气滞血瘀等证型与血黏度等客观指标的相关性探讨.实用中西医结合杂志,1990；3(5)：307.
[64]黑卫可,李娟.冠心病患者血中SOD含量与中医辨证分型的关系.河南中医,1994；14(6)：348-349.
[65]程小曲,刘茂甫,周淑意,等.冠心病及其辨证分型与超氧化物歧化酶过氧化脂质等的关系.实用中西医结合杂志,1998；11(6)：505-506.
[66]孔繁立,兰若,尤松鑫,等.不稳定型心绞痛心肾阳虚证血浆性激素及自由基反应的变化.甘肃中医,1993；6(6)：1-3.
[67]罗俊敏,王国申,王晓宏,等.急性心肌梗塞甲状腺激素变化的临床预后价值.中国综合临床,2001；17(6)：421-422.
[68]谢梦洲,谢英,黄惠勇,等.甲状腺激素在冠心病心气虚证患者血浆中的变化及意义.湖南中医学院学报,2005；25(5)：41-43.
[69]张继东,乔云,武传龙,等.冠心病患者胰.岛素抵抗与中医辨证分型及纤溶系统活性的相关性研究.中国中西医结合杂志,2004；24(5)：408-410.
[70]孔丽君.冠心病患者血浆同型半胱氨酸水平与辨证分型相关性研究.实用中西医结合临床,2004；4(1)：7-8.
[71]方敏,林敏芬,赵新华,等.微波穴位辐射对冠心病患者血流动力学的影响.中华理疗杂志,2000；23(4)：207-209.
[72]杨昌生.冠心病的流行病学和发病机理·安徽医学,1999；(6)：1.
[73]曾凌云。中西医对冠心病病机与治疗的认识进展·中国中医药报,1997-03-10(3).
[74]戴秋孙,沈巧云.实用针灸治疗学.人民卫生出版社,2000；5(1)：221。
[75]程丑夫.冠心病中医诊疗思考[J].湖南中医药大学学报,2009；29(3)：3-5。
[76]程红,罗陆一.江西中医学院学报.2008；20(3)：25-27。
[77]谢感共,赵彩娇,卢献群,等.灵龟八法穴位开闭状态导电量研究.中国针灸,2002；22(5)：315-317.
[78]李友林.实用最佳时间针灸精义.北京：学苑出版社.1994；1：289.
[79]王继红.浅谈灵龟八法的理论渊源及临床运用[J].新中医,2008；40(2)：111-112.
[80]方云鹏,方本正.时间医学与针炙万年历[M].西安陕西科学技术出版社,2001：86.
[81]彭意,周亮.解析灵龟八法之时间医学与理论渊源及创新.广州510405。
[82]孙吉山.奇经纳卦之由来及其发展简史[J].上海针灸杂志,1994；(2)：76.
[83]李磊.传统时间针法的发展简史,传统时间针法.2006；(1)：2-3.
[84]何少初.古代名医解周易[M],北京中国药科技出版社1998,3-4.
[85]谢感共,李红,卢献群,等.灵龟八法针刺治疗窦性心动过速疗效观察.广西中医学院学报,2003；6(4)：7-9.
[86]金嫣莉.电针治疗冠心病心绞痛30例.中国针灸,1987；7(2)：4.
[87]谷安华.灵龟八法结合辨证取穴针刺治疗经前期紧张综合征30例总结[J].湖南中医杂志,2008；24(5)：30.
[88]王家恩,等.针刺治疗冠心病的临床研究.中国针灸,1987；7(2)：5.
[89]龙开平,徐凤琴,张晓军,等.多路循环斩波激光照射对冠心病患者甲襞微循环的影响.微循环学杂志,2007；17(1)：64.
[90]陈可劲,鲁光华,李中和,等.激光血管外及穴位照射治疗冠心病的临床研究[J].实用心脑肺血管病杂志,2006；14(8)：619-620.
[91]杨丹红,等.温灸法治疗冠心病44例临床疗效分析.中国针灸,1989；9(4)：49.
[92]徐俊华,等.针刺合谷穴治疗心绞痛初探.上海针灸杂志,1993；12(3)：101.
[93]巴艳.不同疗法治疗冠心病心绞痛及对血浆ET、CGRP影响的对比研究[J].中医研究,2010：23(6)：75-76.
[94]吴宝庆,刘磊.瓜蒌薤白半夏汤加味和温针灸治疗胸痹26例[J].中外医疗,2007；26(18)：22.
[95]曹建萍.李传杰针药结合治疗冠心病经验[J].中医杂志,2006；47(4)：262-263.
[96]吕金阳.针药结合治疗冠状动脉粥样硬化性心脏病心绞痛62例临床观察[J].河北中医,2007；29(8)：710.
[97]于长义,等.穴位贴药治疗冠心病420例的临床观察中国针灸,1990；10(5)：5。
[98]孔令举,等.针剌治疗冠心病心绞痛28例[J].上海针灸杂志,1996；15(5)：20.
[99]张登部,郑桂秋,侯桂琴,等.艾条悬灸法治疗冠心病138例临床观察[J].中医杂志,1991；32(3)：35-37.
[100]郑桂秋,张登部,刘佩云,等.冠心病的灸治疗法研究[J].中国针灸,1992；12(3)：27-28.
[101]张凤英.微波针灸治疗冠心病心绞痛27例.中级医刊,1995；30(8)：44.
[102]奇峰,姚媛.“温通针法”治疗冠心病49例临床观察.北京中医杂志,2003；22(2)：37-38.
[103]张琳,左林.针刺联合西药治疗冠心病心绞痛的疗效观察.针灸临床杂志,2011；27(2)：27-29.
[104]石向东,赵捷,吕瑛.针灸推拿改善冠心病患者生活质量的临床观察.上海医药,2012；33(10)：37.
[105]毛爱民.背俞穴挑治配合针刺治疗冠心病室性心律失常疗效观察[J].上海 针灸杂志,2010；29(5)：294-295.
[106]Heinrich P C, Castell J V, Andus T. Interleukin-6 and the acute phase response [J]. Biochem J,1990; 265(3):621-636.
[107]劭耕.现代冠心病[M].北京：北京医科大学、中国协和医科大学联合出版社,1994；1-5.
[108]Ross R. Atherosclerosis-an inflammatory disease [J]. N Engl J Med.,1999; 340:115-126.
[109]Ridker P M, Rifai N, Pfeffer M A, et al. Long-term effects of pravastatin on plasma concentration of C-reactive Protein [J]. Circulation,1999; 100:230-235.
[110]Libby P. Inflammation in atherosclerosis [J]. Nature,2002; 420(6917): 868-874.
[111]Bharadwaj D, Stein MP, Volzer M, et al. The major receptor for C-reactive protein on leukocytes is Fcγ reception II [J]. J Exp Med,1999; 190(4):585-590.
[132]Lindahl B, Toss H, Siegbahn A, et al. Markers of myocardial damage and inflammation in relation to long-term mortality in unstable coronary artery disease [J]. N Engl J Med,2000; 343:1139-1147.
[113]Speidl WS, Graf S, Hornykewycz S, et al. High-sensitivity C-reactive protein in the prediction of coronary events in patients with premature coronary artery disease [J]. Am Heart J,2002; 144(3):449-455.
[114]窦克非.冠心病的免疫学机制研究进展[J].中国循环杂志,2003：18(1)：73-75.
[115]Deveraj S, Xu D Y, Jialal I. C-reactive protein increase plasminogen activator inhibitor-1 expression and activity in human aortic endothelial cells: implications for the metabolic syndrome and atherothrombosis [J]. Circulation. 2003; 107:398-404.
[116]Ridker P M, Glynn R J, Hennekens C H. C-reactive protein adds to the predictive value of total and HDL cholesterol in determining risk of first myocardial infarction [J]. Circulation,1998; 97:2007-2011.
[117]Albert M A, Danielson E, Rifai N, et al. Effect of stat in therapy on C-reactive protein levels:The pravastatin inflammation/CRP Evaluation (PRINCE):a randomized trial and cohort study [J]. JAMA,2001:286(1):64-70.
[118]Ridker P M, Cushman M, Stampfer M J, et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men [J]. N Engl J Med, 1997; 336:973-979.
[119]Ikonomidis I, Andreotti F, Economou E, et al. Increased proinflammatory cytokines in patients with chronicstable angina and their reduction by aspirin [J]. Circulation,1999; 100:793-798.
[120]Huittinen T, Leinonen M, Tenkanen L, et al. Synergistic effect of persistent Chlamydia pneumonia infection, autoimmunity, and inflammation on coronary risk [J]. Circulation,2003; 107(2):2566-2571.
[121]Buffon A, Biassucci L M, Liuzzo G, et al. Widespread coronary inflammation in unstable angina [J]. N Engl J Med,2002; 347(1),5-12.
[122]Gearing A J, Newman W. Circulating adhesion molecules in disease [J]. Immunol Today,1993; 14(10):506-512.
[123]Crea F, Biasucci L M, Buffon A, et al. Role of inflammation in the pathogenesis of unstable coronary artery disease [J]. Am J Cardiol,1997; 80(5):10E-16E.
[124]Mulvihill N T, Foley J B, Murphy R, et al. Evidence of prolonged inflammation in unstable angina and non-Q wave myocardial infarction [J]. J Am Coll Cardiol, 2000; 36(4):1210-1216.
[125]Omi H, Okayama N, Shimizu M, et al. Statins inhibit high glucose-mediated neutrophil-endothelial cell adhesion through decreasing surface expression of endothelial adhesion molecules by stimulating production of endothelial nitric oxide [J]. Microvasc Res,2003; 65(2):118-124.
[126]Plutzky J. Atherosclerotic plaque rupture:emerging insights and opportunities [J]. AM J Cardiol,1999; 84(1):15-20.
[127]席嘉宾.冠心病危险因素研究进展[J].卫生职业教育,2005；23(8)：75-76.
[128]Fukuda D, Kawarabayasi T, Tanaka A, et al. Lesion characteristics of acute myocardial infarction:an investigation with intravascular ultrasound [J]. Heart, 2001; 85(4):402-406.
[129]高颖,蔡定芳.基质金属蛋白酶-9与炎症反应研究进展[J].中国病理生理杂志,2003；19(8)：126-129.
[130]张圆圆,张运,张梅,等.辛伐他汀、丙丁酚和卡托普利在动脉粥样硬化斑块消退中的作用及与金属蛋白酶1和组织抑制物1基因表达的关系[J].中国动脉硬化杂志,2003；11(5)：401-404.
[131]Navab M, Berliner J A, Subbanagounder G, et al. HDL and the inflammatory response induced by LDL-derived oxidized phospholipids. Arterioscler Thromb VascBiol,2001; 21:481-488.
[132]van Lenten B J, Navab M, Shih D, et al. The role of high-density lipoproteins in oxidation and inflammation. Trends Cardiovasc Med,2001; 11:155-161.
[133]Yudkin J S, Stehouwer C D, Emeis J J. et al. C-reactive protein in health subjects:association with obesity, insulin resistance, and endothelial dysfunction:a potential role for cytokines originating from adipose tissue? Arterioscler Thromb VascBiol,1999; 19(4):972-978.
[134]Kranzhofer R. Angiotensin induces inflammatory activation of human vascular smooth muscle cells. Arterioscler ThrombVasBoil,1999; 19,1623-1629.
[135]鄭刚.抗血管壁慢性炎症—勤脉粥檬硬化防治的新思路.中西醫结合心腊血管病雜誌,2006；4(2)：143-146.
[136]Dunlop L C, Skinner M P, Bendall L J, et al. Characterization of GMP-140 (P-selectin) as a Circulaing Plasma Protein. J Exp Med,1992; 175(4): 1147-1150.
[137]张均华.血管内皮功能障碍与冠状动脉疾病[J].中华老年心脑血管病杂志,2002；4(1)：3.
[138]孙锡印,杨雯琳.冠心病气滞血癖与气虚血疲证型间血载脂蛋白的异同及辨治影响[J].江苏中医,1997；18(6)：40-41.
[139]Ishiwata N, Takio K, Katayama M, et al. Alternatively spliced isoform of P-selectin is present in vivo as a soluble molecule. The Journal of Biological Chemistry,1994; 269(38),23708-23715.
[140]Miniek C R, Fabricant C G, Fabriant J, et al. Atheroarteroosclerosis induced by infection with a herpesvirus [J]. Am J Pathol,1979; 96:673.
[141]McEver R P, Beckstead J H, Moore K L, et al. GMP-140, a platelet alpha-granule membrane protein, is also synthesized by vascular endothelial cells and is localized in Weibel-Palade Bodies. J. Clin. Invest.1989; 84(1), 92-99.
[142]Macin S M, Perna E R, Farias E F, et al. Atorvastatin has an important acute anti-inflammatory effect in patients with acute coronary syndrome:results of a randomized, double-blind, placebo-controlled study. Am Heart J,2005; 149(3): 451-457.
[143]Albert M A, Danielson E, Ridker P M. Effect of statin therapy on C-reactive protein levels:the pravastatin inflammation/CRP Evaluation (PRINCE):a randomized trial and cohort study [J]. JAMA,2001; 286(1):64-70.
[144]Cannon C P, Braunwald E, McCabe C H, et al. Antibiotic ttreatment of Chlamydia pneumonia after actute coronary syndrome. N Engl J Med,2005: 352(16):1646-1654.
[145]Grayston J T, Kronmal R A, Jackson L A, et al. Azithromycin for the secondary prevention of coronary events. N Engl J Med,2005; 352(16):1637-1645.
[146]Ridker P M, Cushman M, Stampfer M J, et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men [J]. N Engl J Med, 1997; 336(14):973-979.
[147]Ikonomidis I, Andreotti F, Economou E, et al. Increased pro inflammatory cytokines in patients with chronic stable angina and their reduction by aspirin [J]. Circulation,1999:100:793-798.
[148]Hsueh W A, Lyon C J, Quinones M J. Insulin resistance and the endothelium. Am J Med,2004; 117(2):109-117.
[149]Choi D H, Kim S K, Choi S H, et al. Preventive effects of rosiglitazone on restenosis after coronary stent implantation in patient with type 2 diabetes. Diabetes,2004; 27(11):2654-2660.
[150]Freed M I, Ratner R, Marcovina S M, et al. Effect of rosiglitazone alone and in combination with atorvastatin on the metabolic abnormalities of type 2 diabetes mellitues. Am J Cardiol,2002; 90:947-952.
[151]Tillet W S, Franeis T J. Serological reactions in pneumonia with a non-protein somatie faetion of the Pneumoeoeeus. J ExP Med,1930; 52(5):561-564.
[152]许绍强.超敏C反应蛋白在颅脑疾病中的应用价值.现代医学,2007；7(n)：20-22.
[153]Gomes M C. C-reactive Protein:a new golden marker of cardiovascular risk. Rev Port Cardiol,2002,21:1329-1346.
[154]Libby P, Ridker P M, Maseri A. Inflammation and atherosclerosis. Circulation, 2002; 105:1135-1143.
[155]刘刚.冠状动脉硬化患者血清超敏C反应蛋白及胆红素检测的临床意义.蚌埠医学院学报,2007；32(5)：614-615.
[156]万惠,姚伟峰.2型糖尿病大血管病变与超敏C反应蛋白及脂联素相关性研究.右江医学杂志,2006,10,34(5)：13-15.
[157]Liuzzo G, Biasucci L M, Gallimore J R, et al. The prognostic value of C-reactive protein and serum amyloid a protein in severe unstable angina. N Engl J Med,1994; 331(7):417-424.
[158]Pearson T A, Mensah G A, Alexander R W, et al. Makers of information and Cardiovascular disease:applieation to clinieal and publie health practice:a statement for healthcare professionals from the Centers for Disease control and Prevention and the Ameriean Heart Association. Circulation,2003; 107(3): 499-511.
[159]Ferreiros ER, Boissonnet CP, Pizarro R, et al. Independent prognostic value of elevated C-reactive protein in unstable angina. Circulation,1999; 100: 1958-1963.
[160]de Winter R J, Bholasingh R, Lijmer J G, et al. Independent prognostic value of C-reactive protein and troponin I in patients with unstable angina or non-Q-wave myocardial infarction. Cardiovasc Res,1999; 42(1):240-245.
[161]奚耀,钱义明,顾晓刚,等.冠状动脉病变程度和血浆脑钠肤超敏C反应蛋白水平相关性的研究.中国急救医学,2007；27(6)：524-526.
[162]Wilson A M, Ryan M C, Boyle A J. The novel role of C-reactive Protein in cardiovascular disease:risk marker or pathologen. Int J Cardiol,2006,106(3): 291-297.
[163]贾扬地,张其根.血清超敏C反应蛋白水平与心脑血管疾病关系探讨.蚌埠医学院学报,2003,28(5)：453-455.
[164]McCully K. S, Ragsdale B D, Production of arteriosclerosis by homocysteinemia. Am J Pathology.1970; 61(1):1-11.
[165]周伟君,童建菩,叶静,等.超敏C反应蛋白与脑血管疾病危险因素的相关性研究.中国危重病急救医学,2007；19(6)：325-328.
[166]王天成,汪整辉,李国权,等.缺血性脑血管病患者血浆D二聚体和血清同型半肤氨酸、超敏C反应蛋白、总胆红素的变化及相关分析.实用医学杂志,2006；22(13)：1573-1574.
[167]减志忠,潘生英,徐树平,等.急性脑梗死患者治疗前后血清Hcy和hs-CRP检测的临床意义.放射免疫学杂志,2007；20(5)：458-460.
[168]詹建梅,姐德玲.急性脑梗死患者血清超敏C反应蛋白与神经功能缺损的关系.心脑血管病防治,2007；7(5)：334-335.
[169]薛静,吕丽霞.超敏C反应蛋白及血脂与缺血性脑卒中颈动脉粥样硬化的关系.血栓与止血学,2007；13(1)：12-13.
[170]McCully K S. Vascular pathology of homocysteinemia:implications for the pathogenesis of arteriosclerosis. Am J Pathology,1969; 56(1):111-128.
[171]Lentz S R, Rodionov R N, Dayal S. Hyperhomocysteinemia, endothelial dysfunction, and cardiovascular risk:the potential role of ADMA. Atheroscler Suppl.2003,4(4):61-65.
[172]Austin R C, Lentz S R, Werstuck G H. Role of hyperhoocysteinemia in endothelial dysfunction and atherothrombotic disease. Cell Death and Differentiation,2004; 11:s56-s64.
[173]许海燕,陈再嘉,汤健,等.冠心病患者同型半胱氨酸代谢相关酶基因多态性的研究.中华医学杂志,1999；79：414-416.
[174]Gupta A, Moustapha A, Jacobsen D W. et al. High homocysteine, low folate and low vitamin B6 concentrations:prevalant risk factors for vascular disease in heart transplant recipients. Transplantation,1998; 65(4):544-550.
[175]Robinson K, Arheart K, Refsum H, et al. Low circulating folate and vitamin B6 concentrations:risk factors for stroke, peripheral vascular disease, and coronary artery disease. Circulation,1998; 97:437-443.
[176]Boushey C J, Beresford S A, Omenn G S, et al. A quantitative assessment of plasma homocysteine as a risk factor for vascular disease probable benefits of increasing folic acid intakes. JAMA,1995; 274(13):1049-1057.
[177]Selhub J, Jacques P F, Bostom A G, et al. Association between plasma homocysteine concentrations and extracranial carotid-artery stenosis. N Engl J Med,1995; 332:286-291.
[178]Ueland P M. Refsum H. Plasma homocysteine, a risk factor for vascular disease: plasma levels in health, disease, and drug therapy. J Lab Clin Med,1989; 114(5): 473-501.
[179]Welch G N, Loscalzo J, Homocysteine and athero thrombosis. N Eng J Med, 1998; 338:1042-1050.
[180]von Eckardstein A, Assmann G. Plasma homocysteine levels and mortality in patients with coronary artery disease. N Engl J Med,1997; 337:1631-1633.
[181]Ubbink J B, Vermaak W J, Bennett J M, et al. The prevalence of homocysteinemia and hypercholesterolemia in angiographically defined coronary heart disease. Klin Wochenschr,1991; 69(12):527-534.
[182]Ungvarl Z, Sarkadi-Nagy E, Bagi Z, et al. Simultaneously increased TxA2 activity in isolated arterioles and platelets of rats with hyperhomocysteinemia. Arterioscler Thromb Vase Biol,2000; 20(5):1203-1208.
[183]Ling Q, Hajjar K A. Inhibition of endothelial cell thromboresistance by homocysteine. J Natr,2000; 130(2):737-3765.
[184]Moat S J, Lang D, McDowell I F, et al. Folate, homocysteine, endothelial function and cardiovascular disease. J Nutr Biochem,2004; 15(2):64-79.
[185]Ji C, Kaplowitz N. Hyperhomocysteinemia, endoplasmic reticulum stress, and alchoholic liver injury [J]. World J Gastroenterol,2004; 12:1699-1708.
[186]Stangl V, Gunther C, Jarrin A, et al. Homocysteine inhibits TNF-alpha-induced endothelial adhesion molecule expression and monocyte adhesion via nuclear factor-kappaB dependent pathway. Biochem Biophys Res Commun,2001; 280(4):1093-1100.
[187]Wang H, Jiang X, Yang F, et al. Cyclin A transcriptional suppression is the major mechanism mediating homocysteine-induced endothelial cell growth inhibition. Blood,2002; 99(3):939-945.
[188]Hossain G S, van Thienen J V, Werstuck G H, et al. TDAG51 is induced by homocysteine, promotes detachment-mediated programmed cell death, and contributes to the cevelopment of atherosclerosis in hyperhomocyseinemia. J Biol Chem,2003; 278(32):30317-30327.
[189]van Aken B E, Jansen J, van Deventer S J, et al. Elevated levels of homocysteine increase IL-6 production in monocytic mono Mac 6 cells. Blood Coagul & Fibinoiysis,2000; 11:159-164.
[190]Podder R, Sivasbramanian N, DiBello P M, et al. Homocysteine induces expression and secretion of monocyte chemoattractant protein-1 and interleukin-8 in human aortic endothelial cells. Circulation,2001; 103(22): 2717-2723.
[191]Zeng X, Dai J, Remick D G, et al. Homocysteine mediated expression and secretion of monocyte chemoattractant protein-1 and interleukin-8 in human monocytes. Circ Res,2003; 93(4):311-320.
[192]Lange H, Suryapranata H, De Luca G, et al. Folate therapy and in-stent restenosis after coronary stenting. New Engl J Med,2004; 350:2673-2681.
[193]Spencer C G, Martin S C, Felmeden D C, et al. Relationship of homocysteine to markers of platelet and endothelial activation in "high risk" hypertensives:a substudy of the anglo-scandinavian cardiac outcomes trial. Int J Cardiol,2004; 94(2-3):293-300.
[194]Song Y S, Rosenfeld M E. Methionine-induced hyperhomocysteinemia promotes superoxide anion generation and NFkappaB activation in peritoneal macrophages of C57BL/6 mice. J Med Food,2004; 7(2):229-234.
[195]陈宇,王士雯,王宇枚,等.同型半胱氨酸对血管钙化的促进作用.中华心血管病杂志,2003；31(2)：128-131.
[196]李红.按时取穴治疗窦性心动过速即时效应观察.中国针灸,2003；23(3)：132-134.
[197]国际心脏病学会和协会及世界卫生组织临床命名标准化联合专题组.缺血性心脏病的命名及诊断标准.中华心血管病杂志,1981：9(1)：75-76.
[198]陈可冀,寥家祯,肖镇祥.心脑血管疾病研究.上海科学技术出版社,1988,1：316.
[199]中西医结合治疗冠心病心绞痛及心律失常座谈会.冠心病心绞痛及心电图疗效评定标准.医学研究通讯.1979；(12)：17.
[200]国家技术监督局.中医临床诊疗术语证候部分.北京：中国标准出版社,1997：1：20-38.
[201]中华人民共和国卫生部.中药新药临床研究指导原则(第一辑).北京：中国医药科技出版社.1993；68-73.
[202]中国中西医结合学会心血管学会.冠心病中医辨证标准.中西医结合杂志,1991；11(5)：2-7.
[203]中华人民共和国卫生部.中药新药临床研究指导原则(第一辑).北京：中国医药科技出版社,1993；68-73.
[204]文忠荣.浅析“灵龟八法”象数来源[J].中国针灸,2000；(5)：295.
[205]管遵惠.灵龟八法治疗血管神经性头痛80例对比观察[J].云南中医杂志,1987；8(5)：25-27.
[206]管遵惠.杏轩针经[M].昆明·云南科技出版社,2002；174-178.
[207]秦庆云.时间医学.秦庆云大夫个人网站.泰山医学院附属医院中医科.http://www.haodf.com/zhuanjiaguandian/DWTYDFCU_128490.htm
[208]魏晋盛.实用子午流注与灵龟八法临床应用盘人体针灸穴位挂图详解使用说明书2010,7.
[209]廖炼炼.“灵龟八法”针刺治疗中风后遗症的临床观察.四川中医,2008；26(10)：104-106.
[210]林宇凡,陈颖楠,王舰,等.灵龟八法合特效穴治疗中风下肢功能障碍23例临床分析.现代康复,1999；3(2)：197.
[211]谢感共.灵龟八法有关问题的探讨.中南西南针灸学术交流会论文集,1991.
[212]谢感共.灵龟八法的古天文背景.广西针灸学术交流会论文集,1991.
[213]李友林,刘国清.实用最佳时间针灸精义[M].北京：学苑出版社,2005；156.
[214]赵艳玲,唐晨光,章薇,等.针药并用治疗冠心病心绞痛临床疗效观察及对 血浆ET、cGRP影响研究[J].中国针灸,2001；21(2)：70-72.
[215]张玉兰.运用灵龟八法治疗胃脘疼212例疗效观察.针灸临床杂志,1997；13(9)：31.
[216]赵彩娇,谢感共,翁泰来,等.灵龟八法治疗慢性浅表性胃炎临床观察.针灸临床杂志,2002；18(11)：6-7.
[217]高希言,陈雅琴.从穴温改变看灵龟八法选穴.山西中医,1989；(5)：38.
[218]汪桐.经穴时辰节律的皮肤温度电阻改变.陕西中医,1986；(4)：184.
[219]谢感共.灵龟八法穴位开闭状态的研究.中国中医药科技,2002；9(3)：129-131.
[220]谢感共,赵彩娇,卢献群,等灵龟八法穴位开闭状态痛阈值观察.国医论坛,2001；16(6)：47-48.
[221]朱海霞.针刺“内关”等穴治疗心绞痛60例临床观察[J].针灸临床杂,2004；20(10)：38-39.
[2]罗陆一,冯润芬,吴泽民等.温肾化痰活血法心腧穴位外治治疗冠心病心绞痛观察.中医药学刊,2006；24(6)：984-985.
[3]黄梦雨,罗陆一.罗陆一教授治疗冠心病心绞痛经验介绍.新中医杂志,2009：41(11)：13-14.
[4]李磊针.炙时间治疗学.太原：山西科学技术出版社,1994；1.
[5]管遵惠.试论经气的运行.云南中医杂志,1985；3：18.
[6]史裕整理.灵枢经.沈阳：辽宁科学技术出版社,1997.
[7]王冰注.黄帝内经素问.北京：人民卫生出版社,1978.
[8]赵估.圣济总录.北京：人民卫生出版社,1998.
[9]林佩琴.类证治裁.北京：人民卫生出版社,1988.
[10]朱丹溪.丹溪心法.上海：上海科学出版社,1959.
[11]王肯堂.证治准绳.上海：上海科学技术出版社,1984.
[12]叶天士.临证指南医案.上海：上海科学技术出版社,1961.
[13]吴谦.医宗金鉴·订正金匮要略注[M].北京：人民卫生出版社,1982；2：523.
[14]李克光,杨百茀.金匮要略讲义[M].上海：上海科技出版社,1985；94.
[15]梅岩,张明雪.从“阳微阴弦”治冠心病[J].中医药学刊,2006；24(4)：683-684.
[16]张机.金匾要略方论.北京：人民卫生出版社,1978.
[17]赵估.圣济总录.北京：人民卫生出版社,1998.
[18]李十红,等.治疗冠状动脉痉挛心绞痛的经验.辽宁中医杂志,1997；(2)：5.
[19]罗粗文.胸痹心痛临床几个问题探讨.四川中医,1988；(2)：8.
[20]杨利.邓铁涛教授“冠心三论”[J].湖南中医药导报,2004,(6)：8-10.
[21]巢元方.诸病源候论.北京：人民卫生出版社,1984.
[22]林佩琴.类证治裁.北京：人民卫生出版社,1988.
[23]朱文锋.国家标准应用·中医内科疾病诊疗常规[M].长沙：湖南科技出版社,1998：247.
[24]焦树德,路志正.实用中医心病学[M].北京：人民卫生出版,1995；600-616.
[25]丁斗,董小君.气元论在胸痹心痛证治中的病因病机规律研究[J].长春中医药大学学报,2010；26(2)：160-170.
[26]徐健,敖杰男.浅谈痰瘀互结证与胸痹的关系[J].时珍国医国药,2008；18(5)：1229-1230.
[27]王伯东.张景凤自拟方治疗胸痹痰瘀互结证验案举隅[J].吉林中医药,2010； 30(1)：59.
[28]郑玲玲,王强.王强教授治疗痰瘀互结型胸痹临证经验[J].吉林中医药,2012；32(4)：333.
[29]林晓忠.邓铁涛老师调脾护心法治疗冠心病临床经验总结.中国医药学报,2002；17(1)：40.
[30]罗陆一.从肾论治冠心病机理例析.中医药学刊,2005；23(4)：58.
[31]罗粗文.胸痹心痛临床几个问题探讨.四川中医,1988；(2)：8.
[32]李淑贞,等.补肾活血化痰法治疗冠心病心绞痛浅议.实用中医药杂志,2004；20(9)：516.
[33]竺培华,秦志仁.补肾益气活血法治疗冠心病的临床观察.中成药,2004；26(5)：附11.
[34]张永健,俞荣青.对《冠心病(心绞痛、心肌梗塞)中医辨证试行标准》的几点意见[J].中西医结合杂志社,1985；(2)：128.
[35]中医研究院,广东中医学院.中医名词术语选择[M].北京：人民卫生出版社,1973；360.
[36]王永炎.中医内科学[M].上海：上海科技出版社,1997；108-109.
[37]岳美中.岳美中医案集[M].北京：人民卫生出版社,1978；68.
[38]冯润芬,罗陆一.通心贴心俞穴外敷治疗冠心病心绞痛60例临床观察.中国中医药科技,2005；12(1)：47-48.
[39]高彩霞,李冬玉,罗清菊,等.冠心贴膜对冠心病心绞痛患者部分凝血活酶时间和纤维蛋白原水平的影响.河南中医,2005；25(10)：31-32.
[40]龚信.古今医鉴[M].北京：中国中医药出版社,1997；294.
[41]陈寅生,李丽.心脉通贴剂中冰片的透皮吸收实验研究.河南大学学报(医学版),2006；25(1)：30-31.
[42]林晓忠,吴焕林,严夏.邓铁涛教授论治冠心病的规律探要[J].中医药学刊,2001：19(5)412-414.
[43]唐容川.中医内科名著集成[M].北京：华夏出版社,1998；887-888.
[44]黄绳武,宋宵宏.中药复方制剂心安康贴剂的透皮吸收促进剂选择研究.中国药师,2003；6(7)：391-393.
[45]沈建平,丁建花,张银娣,等.保心包贴膜对心肌缺血的影响.中国微循,2002：6(2)：87-91.
[46]张建文,汪大鹏,熊晓玲,等.复方丹参气雾剂治疗冠心病心绞痛的临床观察.湖北中医杂志,2005；27(1)：15-16.
[47]赵锡民.中医药防治肿瘤的研究[J].长春中医药大学学报,2012；28(1)：169-170.
[48]宋丽晶,刘建璇,毋英杰.速效活心气雾剂对麻醉犬心脏功能和血流动力学的影响.长春中医学院学报,2001；17(1)：36-37.
[49]杨发荣.心痛气雾剂治疗冠心病心绞痛100例.辽宁中医杂志,1997；24(8)：355.
[50]王安才,常宝华,杨尚印,等.保心包贴膜对稳定型心绞痛患者血浆内皮素和一氧化氮水平的影响.中国临床药理学与治疗学,2000；5(2)：145-146.
[51]黄伟,郑义通,胡世文.体外超声助溶治疗急性心肌梗死的效果观察.齐齐哈尔医学院学报,2002；23(10)：1108-1109.
[52]刘小斌.邓铁涛教授五脏相关学术源流探讨[J].广州中医药人学学报.2006；23(5)：424-425.
[53]林慧光主编。陈修｜元｜医学全書[M].北京：中国中医药出版社,2003；10：472-474.
[54]郝福庆.拿治疗冠心病70例.实用中医药杂志,2001；17(11)：29.
[55]程国彭.医学心悟[M].北京：人生出版社,2006；6：126.
[56]王兴,魏向春,姜波.血apoA-1,apoB水平与冠心病中医辨证关系的探讨.中医药学报,1991；(1)：46-48.
[57]程小曲.痰浊型冠心病与血脂、脂蛋白、载脂蛋白的关系及痰浊形成机理的探讨.新中医,1994；(3)：7-9.
[58]金志刚,周端,顾仁樾,等.冠心病血瘀证与血清脂蛋白(a)含量的临床观察.河南中医药学刊,1995；10(3)：28-29.
[59]朱晓岚,林院昌,崔志英,等.冠心病的中医辨证与甲皱微循环和血液流变学之间的相关性探讨.第一军医大学学报,1990；10(3)：225-227.
[60]赖真,郭恕,汪建红,等.冠心病心绞痛气虚血瘀和气滞血瘀的微循环变化.湖南中医学院学报,1994；14(3)：44-46.
[61]贾宝善,刘莉,马军,等.冠心病患者血小板膜糖蛋白及血小板功能与中医辨证分型关系的研究.中西医结合杂志,1989；9(12)：717-719.
[62]骆丽娟.冠心病证型与P—选择素、TXB 2及62—Keto—PGF1α含量变化关系的研究.上海中医药杂志,2002；(7)：13-14.
[63]黄文权,罗致强.冠心病气滞血瘀等证型与血黏度等客观指标的相关性探讨.实用中西医结合杂志,1990；3(5)：307.
[64]黑卫可,李娟.冠心病患者血中SOD含量与中医辨证分型的关系.河南中医,1994；14(6)：348-349.
[65]程小曲,刘茂甫,周淑意,等.冠心病及其辨证分型与超氧化物歧化酶过氧化脂质等的关系.实用中西医结合杂志,1998；11(6)：505-506.
[66]孔繁立,兰若,尤松鑫,等.不稳定型心绞痛心肾阳虚证血浆性激素及自由基反应的变化.甘肃中医,1993；6(6)：1-3.
[67]罗俊敏,王国申,王晓宏,等.急性心肌梗塞甲状腺激素变化的临床预后价值.中国综合临床,2001；17(6)：421-422.
[68]谢梦洲,谢英,黄惠勇,等.甲状腺激素在冠心病心气虚证患者血浆中的变化及意义.湖南中医学院学报,2005；25(5)：41-43.
[69]张继东,乔云,武传龙,等.冠心病患者胰.岛素抵抗与中医辨证分型及纤溶系统活性的相关性研究.中国中西医结合杂志,2004；24(5)：408-410.
[70]孔丽君.冠心病患者血浆同型半胱氨酸水平与辨证分型相关性研究.实用中西医结合临床,2004；4(1)：7-8.
[71]方敏,林敏芬,赵新华,等.微波穴位辐射对冠心病患者血流动力学的影响.中华理疗杂志,2000；23(4)：207-209.
[72]杨昌生.冠心病的流行病学和发病机理·安徽医学,1999；(6)：1.
[73]曾凌云。中西医对冠心病病机与治疗的认识进展·中国中医药报,1997-03-10(3).
[74]戴秋孙,沈巧云.实用针灸治疗学.人民卫生出版社,2000；5(1)：221。
[75]程丑夫.冠心病中医诊疗思考[J].湖南中医药大学学报,2009；29(3)：3-5。
[76]程红,罗陆一.江西中医学院学报.2008；20(3)：25-27。
[77]谢感共,赵彩娇,卢献群,等.灵龟八法穴位开闭状态导电量研究.中国针灸,2002；22(5)：315-317.
[78]李友林.实用最佳时间针灸精义.北京：学苑出版社.1994；1：289.
[79]王继红.浅谈灵龟八法的理论渊源及临床运用[J].新中医,2008；40(2)：111-112.
[80]方云鹏,方本正.时间医学与针炙万年历[M].西安陕西科学技术出版社,2001：86.
[81]彭意,周亮.解析灵龟八法之时间医学与理论渊源及创新.广州510405。
[82]孙吉山.奇经纳卦之由来及其发展简史[J].上海针灸杂志,1994；(2)：76.
[83]李磊.传统时间针法的发展简史,传统时间针法.2006；(1)：2-3.
[84]何少初.古代名医解周易[M],北京中国药科技出版社1998,3-4.
[85]谢感共,李红,卢献群,等.灵龟八法针刺治疗窦性心动过速疗效观察.广西中医学院学报,2003；6(4)：7-9.
[86]金嫣莉.电针治疗冠心病心绞痛30例.中国针灸,1987；7(2)：4.
[87]谷安华.灵龟八法结合辨证取穴针刺治疗经前期紧张综合征30例总结[J].湖南中医杂志,2008；24(5)：30.
[88]王家恩,等.针刺治疗冠心病的临床研究.中国针灸,1987；7(2)：5.
[89]龙开平,徐凤琴,张晓军,等.多路循环斩波激光照射对冠心病患者甲襞微循环的影响.微循环学杂志,2007；17(1)：64.
[90]陈可劲,鲁光华,李中和,等.激光血管外及穴位照射治疗冠心病的临床研究[J].实用心脑肺血管病杂志,2006；14(8)：619-620.
[91]杨丹红,等.温灸法治疗冠心病44例临床疗效分析.中国针灸,1989；9(4)：49.
[92]徐俊华,等.针刺合谷穴治疗心绞痛初探.上海针灸杂志,1993；12(3)：101.
[93]巴艳.不同疗法治疗冠心病心绞痛及对血浆ET、CGRP影响的对比研究[J].中医研究,2010：23(6)：75-76.
[94]吴宝庆,刘磊.瓜蒌薤白半夏汤加味和温针灸治疗胸痹26例[J].中外医疗,2007；26(18)：22.
[95]曹建萍.李传杰针药结合治疗冠心病经验[J].中医杂志,2006；47(4)：262-263.
[96]吕金阳.针药结合治疗冠状动脉粥样硬化性心脏病心绞痛62例临床观察[J].河北中医,2007；29(8)：710.
[97]于长义,等.穴位贴药治疗冠心病420例的临床观察中国针灸,1990；10(5)：5。
[98]孔令举,等.针剌治疗冠心病心绞痛28例[J].上海针灸杂志,1996；15(5)：20.
[99]张登部,郑桂秋,侯桂琴,等.艾条悬灸法治疗冠心病138例临床观察[J].中医杂志,1991；32(3)：35-37.
[100]郑桂秋,张登部,刘佩云,等.冠心病的灸治疗法研究[J].中国针灸,1992；12(3)：27-28.
[101]张凤英.微波针灸治疗冠心病心绞痛27例.中级医刊,1995；30(8)：44.
[102]奇峰,姚媛.“温通针法”治疗冠心病49例临床观察.北京中医杂志,2003；22(2)：37-38.
[103]张琳,左林.针刺联合西药治疗冠心病心绞痛的疗效观察.针灸临床杂志,2011；27(2)：27-29.
[104]石向东,赵捷,吕瑛.针灸推拿改善冠心病患者生活质量的临床观察.上海医药,2012；33(10)：37.
[105]毛爱民.背俞穴挑治配合针刺治疗冠心病室性心律失常疗效观察[J].上海 针灸杂志,2010；29(5)：294-295.
[106]Heinrich P C, Castell J V, Andus T. Interleukin-6 and the acute phase response [J]. Biochem J,1990; 265(3):621-636.
[107]劭耕.现代冠心病[M].北京：北京医科大学、中国协和医科大学联合出版社,1994；1-5.
[108]Ross R. Atherosclerosis-an inflammatory disease [J]. N Engl J Med.,1999; 340:115-126.
[109]Ridker P M, Rifai N, Pfeffer M A, et al. Long-term effects of pravastatin on plasma concentration of C-reactive Protein [J]. Circulation,1999; 100:230-235.
[110]Libby P. Inflammation in atherosclerosis [J]. Nature,2002; 420(6917): 868-874.
[111]Bharadwaj D, Stein MP, Volzer M, et al. The major receptor for C-reactive protein on leukocytes is Fcγ reception II [J]. J Exp Med,1999; 190(4):585-590.
[132]Lindahl B, Toss H, Siegbahn A, et al. Markers of myocardial damage and inflammation in relation to long-term mortality in unstable coronary artery disease [J]. N Engl J Med,2000; 343:1139-1147.
[113]Speidl WS, Graf S, Hornykewycz S, et al. High-sensitivity C-reactive protein in the prediction of coronary events in patients with premature coronary artery disease [J]. Am Heart J,2002; 144(3):449-455.
[114]窦克非.冠心病的免疫学机制研究进展[J].中国循环杂志,2003：18(1)：73-75.
[115]Deveraj S, Xu D Y, Jialal I. C-reactive protein increase plasminogen activator inhibitor-1 expression and activity in human aortic endothelial cells: implications for the metabolic syndrome and atherothrombosis [J]. Circulation. 2003; 107:398-404.
[116]Ridker P M, Glynn R J, Hennekens C H. C-reactive protein adds to the predictive value of total and HDL cholesterol in determining risk of first myocardial infarction [J]. Circulation,1998; 97:2007-2011.
[117]Albert M A, Danielson E, Rifai N, et al. Effect of stat in therapy on C-reactive protein levels:The pravastatin inflammation/CRP Evaluation (PRINCE):a randomized trial and cohort study [J]. JAMA,2001:286(1):64-70.
[118]Ridker P M, Cushman M, Stampfer M J, et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men [J]. N Engl J Med, 1997; 336:973-979.
[119]Ikonomidis I, Andreotti F, Economou E, et al. Increased proinflammatory cytokines in patients with chronicstable angina and their reduction by aspirin [J]. Circulation,1999; 100:793-798.
[120]Huittinen T, Leinonen M, Tenkanen L, et al. Synergistic effect of persistent Chlamydia pneumonia infection, autoimmunity, and inflammation on coronary risk [J]. Circulation,2003; 107(2):2566-2571.
[121]Buffon A, Biassucci L M, Liuzzo G, et al. Widespread coronary inflammation in unstable angina [J]. N Engl J Med,2002; 347(1),5-12.
[122]Gearing A J, Newman W. Circulating adhesion molecules in disease [J]. Immunol Today,1993; 14(10):506-512.
[123]Crea F, Biasucci L M, Buffon A, et al. Role of inflammation in the pathogenesis of unstable coronary artery disease [J]. Am J Cardiol,1997; 80(5):10E-16E.
[124]Mulvihill N T, Foley J B, Murphy R, et al. Evidence of prolonged inflammation in unstable angina and non-Q wave myocardial infarction [J]. J Am Coll Cardiol, 2000; 36(4):1210-1216.
[125]Omi H, Okayama N, Shimizu M, et al. Statins inhibit high glucose-mediated neutrophil-endothelial cell adhesion through decreasing surface expression of endothelial adhesion molecules by stimulating production of endothelial nitric oxide [J]. Microvasc Res,2003; 65(2):118-124.
[126]Plutzky J. Atherosclerotic plaque rupture:emerging insights and opportunities [J]. AM J Cardiol,1999; 84(1):15-20.
[127]席嘉宾.冠心病危险因素研究进展[J].卫生职业教育,2005；23(8)：75-76.
[128]Fukuda D, Kawarabayasi T, Tanaka A, et al. Lesion characteristics of acute myocardial infarction:an investigation with intravascular ultrasound [J]. Heart, 2001; 85(4):402-406.
[129]高颖,蔡定芳.基质金属蛋白酶-9与炎症反应研究进展[J].中国病理生理杂志,2003；19(8)：126-129.
[130]张圆圆,张运,张梅,等.辛伐他汀、丙丁酚和卡托普利在动脉粥样硬化斑块消退中的作用及与金属蛋白酶1和组织抑制物1基因表达的关系[J].中国动脉硬化杂志,2003；11(5)：401-404.
[131]Navab M, Berliner J A, Subbanagounder G, et al. HDL and the inflammatory response induced by LDL-derived oxidized phospholipids. Arterioscler Thromb VascBiol,2001; 21:481-488.
[132]van Lenten B J, Navab M, Shih D, et al. The role of high-density lipoproteins in oxidation and inflammation. Trends Cardiovasc Med,2001; 11:155-161.
[133]Yudkin J S, Stehouwer C D, Emeis J J. et al. C-reactive protein in health subjects:association with obesity, insulin resistance, and endothelial dysfunction:a potential role for cytokines originating from adipose tissue? Arterioscler Thromb VascBiol,1999; 19(4):972-978.
[134]Kranzhofer R. Angiotensin induces inflammatory activation of human vascular smooth muscle cells. Arterioscler ThrombVasBoil,1999; 19,1623-1629.
[135]鄭刚.抗血管壁慢性炎症—勤脉粥檬硬化防治的新思路.中西醫结合心腊血管病雜誌,2006；4(2)：143-146.
[136]Dunlop L C, Skinner M P, Bendall L J, et al. Characterization of GMP-140 (P-selectin) as a Circulaing Plasma Protein. J Exp Med,1992; 175(4): 1147-1150.
[137]张均华.血管内皮功能障碍与冠状动脉疾病[J].中华老年心脑血管病杂志,2002；4(1)：3.
[138]孙锡印,杨雯琳.冠心病气滞血癖与气虚血疲证型间血载脂蛋白的异同及辨治影响[J].江苏中医,1997；18(6)：40-41.
[139]Ishiwata N, Takio K, Katayama M, et al. Alternatively spliced isoform of P-selectin is present in vivo as a soluble molecule. The Journal of Biological Chemistry,1994; 269(38),23708-23715.
[140]Miniek C R, Fabricant C G, Fabriant J, et al. Atheroarteroosclerosis induced by infection with a herpesvirus [J]. Am J Pathol,1979; 96:673.
[141]McEver R P, Beckstead J H, Moore K L, et al. GMP-140, a platelet alpha-granule membrane protein, is also synthesized by vascular endothelial cells and is localized in Weibel-Palade Bodies. J. Clin. Invest.1989; 84(1), 92-99.
[142]Macin S M, Perna E R, Farias E F, et al. Atorvastatin has an important acute anti-inflammatory effect in patients with acute coronary syndrome:results of a randomized, double-blind, placebo-controlled study. Am Heart J,2005; 149(3): 451-457.
[143]Albert M A, Danielson E, Ridker P M. Effect of statin therapy on C-reactive protein levels:the pravastatin inflammation/CRP Evaluation (PRINCE):a randomized trial and cohort study [J]. JAMA,2001; 286(1):64-70.
[144]Cannon C P, Braunwald E, McCabe C H, et al. Antibiotic ttreatment of Chlamydia pneumonia after actute coronary syndrome. N Engl J Med,2005: 352(16):1646-1654.
[145]Grayston J T, Kronmal R A, Jackson L A, et al. Azithromycin for the secondary prevention of coronary events. N Engl J Med,2005; 352(16):1637-1645.
[146]Ridker P M, Cushman M, Stampfer M J, et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men [J]. N Engl J Med, 1997; 336(14):973-979.
[147]Ikonomidis I, Andreotti F, Economou E, et al. Increased pro inflammatory cytokines in patients with chronic stable angina and their reduction by aspirin [J]. Circulation,1999:100:793-798.
[148]Hsueh W A, Lyon C J, Quinones M J. Insulin resistance and the endothelium. Am J Med,2004; 117(2):109-117.
[149]Choi D H, Kim S K, Choi S H, et al. Preventive effects of rosiglitazone on restenosis after coronary stent implantation in patient with type 2 diabetes. Diabetes,2004; 27(11):2654-2660.
[150]Freed M I, Ratner R, Marcovina S M, et al. Effect of rosiglitazone alone and in combination with atorvastatin on the metabolic abnormalities of type 2 diabetes mellitues. Am J Cardiol,2002; 90:947-952.
[151]Tillet W S, Franeis T J. Serological reactions in pneumonia with a non-protein somatie faetion of the Pneumoeoeeus. J ExP Med,1930; 52(5):561-564.
[152]许绍强.超敏C反应蛋白在颅脑疾病中的应用价值.现代医学,2007；7(n)：20-22.
[153]Gomes M C. C-reactive Protein:a new golden marker of cardiovascular risk. Rev Port Cardiol,2002,21:1329-1346.
[154]Libby P, Ridker P M, Maseri A. Inflammation and atherosclerosis. Circulation, 2002; 105:1135-1143.
[155]刘刚.冠状动脉硬化患者血清超敏C反应蛋白及胆红素检测的临床意义.蚌埠医学院学报,2007；32(5)：614-615.
[156]万惠,姚伟峰.2型糖尿病大血管病变与超敏C反应蛋白及脂联素相关性研究.右江医学杂志,2006,10,34(5)：13-15.
[157]Liuzzo G, Biasucci L M, Gallimore J R, et al. The prognostic value of C-reactive protein and serum amyloid a protein in severe unstable angina. N Engl J Med,1994; 331(7):417-424.
[158]Pearson T A, Mensah G A, Alexander R W, et al. Makers of information and Cardiovascular disease:applieation to clinieal and publie health practice:a statement for healthcare professionals from the Centers for Disease control and Prevention and the Ameriean Heart Association. Circulation,2003; 107(3): 499-511.
[159]Ferreiros ER, Boissonnet CP, Pizarro R, et al. Independent prognostic value of elevated C-reactive protein in unstable angina. Circulation,1999; 100: 1958-1963.
[160]de Winter R J, Bholasingh R, Lijmer J G, et al. Independent prognostic value of C-reactive protein and troponin I in patients with unstable angina or non-Q-wave myocardial infarction. Cardiovasc Res,1999; 42(1):240-245.
[161]奚耀,钱义明,顾晓刚,等.冠状动脉病变程度和血浆脑钠肤超敏C反应蛋白水平相关性的研究.中国急救医学,2007；27(6)：524-526.
[162]Wilson A M, Ryan M C, Boyle A J. The novel role of C-reactive Protein in cardiovascular disease:risk marker or pathologen. Int J Cardiol,2006,106(3): 291-297.
[163]贾扬地,张其根.血清超敏C反应蛋白水平与心脑血管疾病关系探讨.蚌埠医学院学报,2003,28(5)：453-455.
[164]McCully K. S, Ragsdale B D, Production of arteriosclerosis by homocysteinemia. Am J Pathology.1970; 61(1):1-11.
[165]周伟君,童建菩,叶静,等.超敏C反应蛋白与脑血管疾病危险因素的相关性研究.中国危重病急救医学,2007；19(6)：325-328.
[166]王天成,汪整辉,李国权,等.缺血性脑血管病患者血浆D二聚体和血清同型半肤氨酸、超敏C反应蛋白、总胆红素的变化及相关分析.实用医学杂志,2006；22(13)：1573-1574.
[167]减志忠,潘生英,徐树平,等.急性脑梗死患者治疗前后血清Hcy和hs-CRP检测的临床意义.放射免疫学杂志,2007；20(5)：458-460.
[168]詹建梅,姐德玲.急性脑梗死患者血清超敏C反应蛋白与神经功能缺损的关系.心脑血管病防治,2007；7(5)：334-335.
[169]薛静,吕丽霞.超敏C反应蛋白及血脂与缺血性脑卒中颈动脉粥样硬化的关系.血栓与止血学,2007；13(1)：12-13.
[170]McCully K S. Vascular pathology of homocysteinemia:implications for the pathogenesis of arteriosclerosis. Am J Pathology,1969; 56(1):111-128.
[171]Lentz S R, Rodionov R N, Dayal S. Hyperhomocysteinemia, endothelial dysfunction, and cardiovascular risk:the potential role of ADMA. Atheroscler Suppl.2003,4(4):61-65.
[172]Austin R C, Lentz S R, Werstuck G H. Role of hyperhoocysteinemia in endothelial dysfunction and atherothrombotic disease. Cell Death and Differentiation,2004; 11:s56-s64.
[173]许海燕,陈再嘉,汤健,等.冠心病患者同型半胱氨酸代谢相关酶基因多态性的研究.中华医学杂志,1999；79：414-416.
[174]Gupta A, Moustapha A, Jacobsen D W. et al. High homocysteine, low folate and low vitamin B6 concentrations:prevalant risk factors for vascular disease in heart transplant recipients. Transplantation,1998; 65(4):544-550.
[175]Robinson K, Arheart K, Refsum H, et al. Low circulating folate and vitamin B6 concentrations:risk factors for stroke, peripheral vascular disease, and coronary artery disease. Circulation,1998; 97:437-443.
[176]Boushey C J, Beresford S A, Omenn G S, et al. A quantitative assessment of plasma homocysteine as a risk factor for vascular disease probable benefits of increasing folic acid intakes. JAMA,1995; 274(13):1049-1057.
[177]Selhub J, Jacques P F, Bostom A G, et al. Association between plasma homocysteine concentrations and extracranial carotid-artery stenosis. N Engl J Med,1995; 332:286-291.
[178]Ueland P M. Refsum H. Plasma homocysteine, a risk factor for vascular disease: plasma levels in health, disease, and drug therapy. J Lab Clin Med,1989; 114(5): 473-501.
[179]Welch G N, Loscalzo J, Homocysteine and athero thrombosis. N Eng J Med, 1998; 338:1042-1050.
[180]von Eckardstein A, Assmann G. Plasma homocysteine levels and mortality in patients with coronary artery disease. N Engl J Med,1997; 337:1631-1633.
[181]Ubbink J B, Vermaak W J, Bennett J M, et al. The prevalence of homocysteinemia and hypercholesterolemia in angiographically defined coronary heart disease. Klin Wochenschr,1991; 69(12):527-534.
[182]Ungvarl Z, Sarkadi-Nagy E, Bagi Z, et al. Simultaneously increased TxA2 activity in isolated arterioles and platelets of rats with hyperhomocysteinemia. Arterioscler Thromb Vase Biol,2000; 20(5):1203-1208.
[183]Ling Q, Hajjar K A. Inhibition of endothelial cell thromboresistance by homocysteine. J Natr,2000; 130(2):737-3765.
[184]Moat S J, Lang D, McDowell I F, et al. Folate, homocysteine, endothelial function and cardiovascular disease. J Nutr Biochem,2004; 15(2):64-79.
[185]Ji C, Kaplowitz N. Hyperhomocysteinemia, endoplasmic reticulum stress, and alchoholic liver injury [J]. World J Gastroenterol,2004; 12:1699-1708.
[186]Stangl V, Gunther C, Jarrin A, et al. Homocysteine inhibits TNF-alpha-induced endothelial adhesion molecule expression and monocyte adhesion via nuclear factor-kappaB dependent pathway. Biochem Biophys Res Commun,2001; 280(4):1093-1100.
[187]Wang H, Jiang X, Yang F, et al. Cyclin A transcriptional suppression is the major mechanism mediating homocysteine-induced endothelial cell growth inhibition. Blood,2002; 99(3):939-945.
[188]Hossain G S, van Thienen J V, Werstuck G H, et al. TDAG51 is induced by homocysteine, promotes detachment-mediated programmed cell death, and contributes to the cevelopment of atherosclerosis in hyperhomocyseinemia. J Biol Chem,2003; 278(32):30317-30327.
[189]van Aken B E, Jansen J, van Deventer S J, et al. Elevated levels of homocysteine increase IL-6 production in monocytic mono Mac 6 cells. Blood Coagul & Fibinoiysis,2000; 11:159-164.
[190]Podder R, Sivasbramanian N, DiBello P M, et al. Homocysteine induces expression and secretion of monocyte chemoattractant protein-1 and interleukin-8 in human aortic endothelial cells. Circulation,2001; 103(22): 2717-2723.
[191]Zeng X, Dai J, Remick D G, et al. Homocysteine mediated expression and secretion of monocyte chemoattractant protein-1 and interleukin-8 in human monocytes. Circ Res,2003; 93(4):311-320.
[192]Lange H, Suryapranata H, De Luca G, et al. Folate therapy and in-stent restenosis after coronary stenting. New Engl J Med,2004; 350:2673-2681.
[193]Spencer C G, Martin S C, Felmeden D C, et al. Relationship of homocysteine to markers of platelet and endothelial activation in "high risk" hypertensives:a substudy of the anglo-scandinavian cardiac outcomes trial. Int J Cardiol,2004; 94(2-3):293-300.
[194]Song Y S, Rosenfeld M E. Methionine-induced hyperhomocysteinemia promotes superoxide anion generation and NFkappaB activation in peritoneal macrophages of C57BL/6 mice. J Med Food,2004; 7(2):229-234.
[195]陈宇,王士雯,王宇枚,等.同型半胱氨酸对血管钙化的促进作用.中华心血管病杂志,2003；31(2)：128-131.
[196]李红.按时取穴治疗窦性心动过速即时效应观察.中国针灸,2003；23(3)：132-134.
[197]国际心脏病学会和协会及世界卫生组织临床命名标准化联合专题组.缺血性心脏病的命名及诊断标准.中华心血管病杂志,1981：9(1)：75-76.
[198]陈可冀,寥家祯,肖镇祥.心脑血管疾病研究.上海科学技术出版社,1988,1：316.
[199]中西医结合治疗冠心病心绞痛及心律失常座谈会.冠心病心绞痛及心电图疗效评定标准.医学研究通讯.1979；(12)：17.
[200]国家技术监督局.中医临床诊疗术语证候部分.北京：中国标准出版社,1997：1：20-38.
[201]中华人民共和国卫生部.中药新药临床研究指导原则(第一辑).北京：中国医药科技出版社.1993；68-73.
[202]中国中西医结合学会心血管学会.冠心病中医辨证标准.中西医结合杂志,1991；11(5)：2-7.
[203]中华人民共和国卫生部.中药新药临床研究指导原则(第一辑).北京：中国医药科技出版社,1993；68-73.
[204]文忠荣.浅析“灵龟八法”象数来源[J].中国针灸,2000；(5)：295.
[205]管遵惠.灵龟八法治疗血管神经性头痛80例对比观察[J].云南中医杂志,1987；8(5)：25-27.
[206]管遵惠.杏轩针经[M].昆明·云南科技出版社,2002；174-178.
[207]秦庆云.时间医学.秦庆云大夫个人网站.泰山医学院附属医院中医科.http://www.haodf.com/zhuanjiaguandian/DWTYDFCU_128490.htm
[208]魏晋盛.实用子午流注与灵龟八法临床应用盘人体针灸穴位挂图详解使用说明书2010,7.
[209]廖炼炼.“灵龟八法”针刺治疗中风后遗症的临床观察.四川中医,2008；26(10)：104-106.
[210]林宇凡,陈颖楠,王舰,等.灵龟八法合特效穴治疗中风下肢功能障碍23例临床分析.现代康复,1999；3(2)：197.
[211]谢感共.灵龟八法有关问题的探讨.中南西南针灸学术交流会论文集,1991.
[212]谢感共.灵龟八法的古天文背景.广西针灸学术交流会论文集,1991.
[213]李友林,刘国清.实用最佳时间针灸精义[M].北京：学苑出版社,2005；156.
[214]赵艳玲,唐晨光,章薇,等.针药并用治疗冠心病心绞痛临床疗效观察及对 血浆ET、cGRP影响研究[J].中国针灸,2001；21(2)：70-72.
[215]张玉兰.运用灵龟八法治疗胃脘疼212例疗效观察.针灸临床杂志,1997；13(9)：31.
[216]赵彩娇,谢感共,翁泰来,等.灵龟八法治疗慢性浅表性胃炎临床观察.针灸临床杂志,2002；18(11)：6-7.
[217]高希言,陈雅琴.从穴温改变看灵龟八法选穴.山西中医,1989；(5)：38.
[218]汪桐.经穴时辰节律的皮肤温度电阻改变.陕西中医,1986；(4)：184.
[219]谢感共.灵龟八法穴位开闭状态的研究.中国中医药科技,2002；9(3)：129-131.
[220]谢感共,赵彩娇,卢献群,等灵龟八法穴位开闭状态痛阈值观察.国医论坛,2001；16(6)：47-48.
[221]朱海霞.针刺“内关”等穴治疗心绞痛60例临床观察[J].针灸临床杂,2004；20(10)：38-39.